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1
Respiratory Mechanisms
in Acid - Base Homeostasis
Assoc. Prof. Faridah Abdul RashidDept. of Chemical Pathology
School of Medical SciencesUSM Kubang Kerian, Kelantan
Medicine 2004/2005
Phase 1, Year 1
Respiratory Block, Week 2
Saturday, 26 February 2005, 8:30 am ± 9:30 am, DK4
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Part 1
� Normal values for arterial blood gases
� Carbonic acid/bicarbonate buffer system
� Henderson-Hasselbalch equation
Own reading
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Memorise
Normal values for arterial blood gases
Blood Gas Parameter Parameter Reported
and Symbol Used
Normal Value
Carbon dioxide
tension*
PCO2 35 ± 45 mm Hg
(average, 40)
Oxygen tension* PO2 80 ± 100 mm Hg
Oxygen percent
saturation
SO2 97
Hydrogen ion
concentration*
pH 7.35 ± 7.45
Bicarbonate HCO3- 22 ± 26 mmol/L
Arterial Blood Gases (ABG)
* Indicates measured parameter Normal values may differ slightly in exams
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Carbonic acid/bicarbonate buffer system
� Carbonic acid is formed when CO2 combineswith water. This reaction is catalysed bycarbonic anhydrase
� Carbonic acid dissociates spontaneously to forma proton and a bicarbonate ion
� The above reactions are reversible:± Write the reaction for buffering acids formed in tissues
± Write the reaction for CO2 release in the lungs
CO2 + H2O ' H2CO3' H+ + HCO3-
Gold
trunk
CA
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Carbonic acid/bicarbonate buffer system
� Carbonic acid is a weak acid� Carbonic acid dissociates spontaneously to form
a proton and a bicarbonate ion
� The pKa of carbonic acid is 6.1
� Carbonic acid is the major buffer in ECF
� The pH of blood can be determined using theHenderson-Hasselbalch equation
H2CO3 ' H+ + HCO3-
Carbonic acid Bicarbonate ion
pKa = 6.1
ECF:
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� pH = pKa + log [HCO3-]/[H2CO3]
� pH = pKa + log [HCO3-]/0.03 x PCO2
� pH = 6.1 + log [HCO3
-
]/0.03 x PCO2
� 7.4 = 6.1 + log 20/1
� 7.4 = 6.1 + 1.3
� The solubility constant of CO2 is 0.03� The pKa of carbonic acid is 6.1
� Plasma pH equals 7.4 when buffer ratio is 20/1
� Plasma pH may be affected by a change in either the bicarbonateconcentration or the PCO
2
� The [HCO3-] and PCO2 values determine plasma pH
Memorise
Henderson-Hasselbalch equation
Gold trunk
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Part 2
� CO2 and PCO2
± Pulmonary function & CO2 homeostasis
± CO2 elimination
� Hyperventilation± Lowering PCO2
± Alveolar hyperventilation
± Causes of alveolar hyperventilation
� Hypoventilation± Raising PCO2
± Alveolar hypoventilation
± Causes of alveolar hypoventilation
Own reading
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CO2 and PCO2
� The amount of CO2 in the blood is directly
related to the PCO2
� The CO2 dissociation curve is nearly linear in the physiologic range of PCO2
� There is never any significant barrier to
CO2
diffusion; CO2
diffuses freely
� PCO2 provides a good index of the
adequacy of ventilation
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Pulmonary Ventilation
� Normal, unassisted breathing:
± An increase in arterial P CO2 acts through therespiratory centre to increase the rate of
pulmonary ventilation± A decrease in arterial P CO2 reduces the rate
of ventilation
� Assisted breathing:
± A respirator is used to assist breathing byexpelling CO2, thus reducing PCO2 in blood
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Pulmonary function & CO2 homeostasis
� The acid-base balance of the body is greatly affected bypulmonary function and CO2 homeostasis:
CO2 homeostasis
[H2CO3] [HCO3-]
CO2 + H2O ' H2CO3 ' H+ + HCO3-
1:20
Normalpulmonary function
Normal acid-base balance; pH remains at 7.4
Normal bicarbonate/carbonic acid ratio
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CO2 elimination
� CO2 elimination through the lungs must be
matched with CO2 production for adequate
ventilation
� CO2 is highly diffusible:
± CO2 tensions are equal in alveolar air and
arterial blood
± Thus, PCO2 is the direct and immediate
reflection of the alveolar ventilation in relation
to the metabolic rate
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Hyperventilation� Hyperventilation (alveolar ventilation in excess of
metabolic needs) causes alkalosis (o in blood pH above
the normal 7.4) as a result of the excess excretion of CO2
from the lungs
Pulmonary function
Hyperventilation
CO2 homeostasis
q CO2, q PCO2
Acid-base disorder
Alkalosis
[H2CO3][HCO3
-
]
CO2 + H2O ' H2CO3 ' H+ + HCO3-
1:>20
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Lowering PCO2
� Lowering the PCO2, as in hyperventilation, causes the
reaction to proceed to the left, with consequent lowering
of the H+ concentration (elevated pH)
Reaction shifts left
Hyperventilation
Excess excretion of
CO2 from the lungs
q CO2, q PCO2
CO2 + H2O ' H2CO3 ' H+ + HCO3-
Reaction shifts left
q [H+], o pH, alkalosis
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Alveolar hyperventilation
� The direct cause of a lowered PCO2 isalways alveolar hyperventilation
� Hyperventilation causes respiratoryalkalosis and a rise in the pH of the blood
� Hyperventilation represents an effort toraise the PO2 at the expense of excretingexcess CO2 from the lungs
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Causes of alveolar hyperventilation
� Hyperventilation is common in:
± asthma
± pneumonia
� Hyperventilation may also be caused by:
± brain injury
± tumour
± aspirin poisoning± anxiety
� Hyperventilation may be a compensationfor metabolic acidosis
Gold trunk
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Hypoventilation� Hypoventilation (alveolar ventilation insufficient to meet
metabolic needs) causes acidosis (decrease of the blood
pH below the normal 7.4) as a result of the retention of
CO2 by the lungs
Pulmonary function
Hypoventilation
CO2 homeostasiso CO2, o PCO2
Acid-base disorder
Acidosis
[H2CO3]
[HCO3
-
]
CO2 + H2O ' H2CO3 ' H+ + HCO3-
1:<20
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Raising PCO2
� Raising the PCO2, as in hypoventilation, causes the
reaction to proceed to the right, producing an increase in
H+ concentration (decreased pH)
Reaction shifts right
Hypoventilation
Retention of CO2 by
the lungs
o CO2, o PCO2
CO2 + H2O ' H2CO3 ' H+ + HCO3-
Reaction shifts right
o [H+], q pH, acidosis
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Alveolar hypoventilation
� When PCO2 rises, the direct cause isalways generalised alveolar hypoventilation
� Hypoventilation causes respiratoryacidosis and a fall in the pH of the blood
� Alveolar hypoventilation may occur if therespiratory rate is decreased
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Causes of alveolar hypoventilation
� Hypoventilation occurs in many conditions thataffect the respiratory system
� CO2 retention is caused by trapped air in the
lungs as occurs in:± emphysema
± chronic bronchitis
� Alveolar hypoventilation may occur in:± narcotic
± barbiturate drug overdose
� The PCO2 may also rise to compensate for metabolic alkalosis
Gold trunk
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Alveolar hypoventilation
� To interpret the PCO2 correctly, one must
also consider the blood pH and
bicarbonate levels to determine whether a
change is caused by a primary respiratory
condition or is compensating for a
metabolic condition
SUMMARY
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Pulmonary functionHyperventilation
Hypoventilation
CO2 homeostasisqCO2, q PCO2
o CO2, o PCO2
Acid-base disorders
Alkalosis
Acidosis
[H2CO3]
[HCO3
-
]
CO2 + H2O ' H2CO3 ' H+ + HCO3-
1:20
Bicarbonate/carbonic acid ratio
>20:1
<20:1
SUMMARY Gold trunk
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Equivalences
Disorder Cause Mechanism
Respiratory
acidosis
Hypercapnia Alveolar
hypoventilation
q pH oo PCO2 CO2 retention
Respiratoryalkalosis
Hypocapnia Alveolar hyperventilation
o pH qq PCO2 blow off CO2
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Part 3
� Acid-base disturbances: Types of acid-base imbalance1. Respiratory acidosis
2. Respiratory alkalosis
3. Metabolic acidosis
4. Metabolic alkalosis
� Acid-base changes in acidosis & alkalosis andcompensation
± T erms used for describing compensation
± R enal compensatory mechanisms in acid-base imbalance± Metabolic and respiratory acid-base changes in blood
± Compensation in respiratory disorders
± Compensation in metabolic disorders
Own reading
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Acid-base disturbances
� pH = 6.1 + log [HCO3-]/0.03 x PCO2
� Plasma pH may be affected by a changein either the [bicarbonate] or the PCO2:± When the primary change is in the PCO2, the
disturbance is called respiratory; when it is the
[bicarbonate], it is called metabolic:
� o PCO2 will decrease pH
� q PCO2 will increase pH
� q HCO3- will decrease pH
� o HCO3- will increase pH
Respiratory
Metabolic
acidosis
alkalosis
acidosis
alkalosis
Memorise
Gold trunk
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Types of acid-base imbalance
� S imple acid-base imbalance:1. Respiratory acidosis
2. Respiratory alkalosis
3. Metabolic acidosis4. Metabolic alkalosis
� M ixed acid-base imbalance
± R efer to:-Interpretation of Diagnostic Tests. Seventh Edition, 2000
Jacques Wallach
Lippincott Williams & Wilkins, Philadelphia
Chapter 12 ± Acid-Base Disorders, pages 489-500
(P hase 1 MD)
(P hase 2 MD)
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Acid-base changes in acidosis and alkalosis
Acid-base Disturbance pH HCO3- PCO2
Respiratory acidosis q o
oRespiratory alkalosis o q q
Metabolic acidosis qq
q
Metabolic alkalosis o o o
Thicker arrows indicate primary disorder
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Memorise
Acid-base changes in acidosis and alkalosis
Acid-base Disturbance pH HCO3- PCO2
Respiratory acidosis q o o
Respiratory alkalosis o q q
Metabolic acidosis q q q
Metabolic alkalosis o o o
Thicker arrows indicate primary disorder
pH, HCO3-
in samedirection;
PCO2
will follow
HCO3-
pH, PCO2 in
oppositedirections;
HCO3- will
follow PCO2
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Compensation
� The purpose of the compensation is to return theblood pH to normal
� The change in the PCO2 in the metabolicdisorders represents the lung¶s role incompensation
� The change in the bicarbonate level representsthe kidney¶s attempt to compensate for therespiratory acidosis or alkalosis
Gold trunk
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Respiratory Compensation for
Preventing Change in pH
Acidosis
CO2 o
H+o
Acidaemia
pH q, PCO2 o
CO2 removal
Via respiration
Normal pH
Normal or o CO2 removal
Slow or q CO2 removal
Cells/Tissue Blood
Lungs
Blood
H ypoventilate
H yperventilate
Acidosis may be accompanied by acidaemia.
The change in pH may be prevented by respiratory removal of CO2.
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Respiratory Compensation for
Preventing Change in pH
Alkalosis
CO2 q
HCO3-o
Alkalaemia
pH o, PCO2 q, HCO3-o
CO2 retention
Via respiration
Normal pH
Normal or o CO2 retention
Slow or q CO2 retention
Cells/Tissue Blood
Lungs
BloodH
ypoventilate
H yperventilate
Alkalosis will not be accompanied by alkalaemia
if enough CO2 has been retained to prevent the change in pH.
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Compensation in respiratory disorders
� Compensation in respiratory disorders is a two-phase process:
(i) Acute response: initial 10 minutes
� Involves blood buffers
(ii) C hronic (renal) adaptation: for up to 4-8 days
� The change in the bicarbonate level represents the kidney¶sattempt to compensate for the respiratory acidosis or alkalosis
� pH returns towards normal but not pH 7.4:
pH 7.7
pH 7.6pH 7.5
pH 7.4
pH 7.3
pH 7.2
pH 7.1
RESPIRATORY ACIDOSIS
Acute response pH 7.1p7.2Chronic response pH 7.2p7.35 RESPIRATORY ALKALOSIS
Acute response pH 7.7p7.6
Chronic response pH 7.6p7.45
4 days 8 days
10 min
10 min
Gold trunk
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Compensation in respiratory disorders
1. Compensation in respiratory disorders is a two-phase process:
(i) Acute response occurs during initial 10 minutes
� This buffering by buffers in blood
� Changes in [HCO3-] occur within 10 minutes
(ii)C
hronic (renal) adaptation occurs for up to 4-8 days� The change in the bicarbonate level represents the kidney¶s
attempt to compensate for the respiratory acidosis or alkalosis
� Changes in [HCO3-] occur up to:
» 4 days in respiratory acidosis
» 8 days in respiratory alkalosis
2. Changes in [HCO3-] and pH occur within 10 minutes, and up to:
4 days in respiratory acidosis
8 days in respiratory alkalosis
Gold trunk
Changes in bicarbonate
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Compensation in respiratory disorders
1. Compensation in respiratory disorders is a two-phase process:
(i) Acute response occurs during initial 10 minutes
� This buffering by buffers in blood
� Changes in pH occur within 10 minutes
(ii) C hronic (renal) adaptation occurs for up to 4-8 days
� Changes in pH occur up to:
» 4 days in respiratory acidosis
» 8 days in respiratory alkalosis
2. Changes in pH occur within 10 minutes, and up to:
4 days in respiratory acidosis8 days in respiratory alkalosis
3. pH returns towards normal but not pH 7.4:
Final pH 7.35 in respiratory acidosis
Final pH 7.45 in respiratory alkalosis
Gold trunk1. Summary of changes in pH
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Compensation in respiratory disorders
1. Compensation in respiratory disorders is a two-phase process
2. Changes in pH occur within 10 minutes, and up to:
(i) 4 days in respiratory acidosis
(ii) 8 days in respiratory alkalosis
3. When fully compensated, pH returns towards normal but not pH 7.4
4. pH Changes in RESPIRATORY ACIDOSIS are:
(i) Acute response pH 7.1p7.2 (initial 10 minutes)(ii) Chronic response pH 7.2p7.35 (lower normal limit within 4 days)
5. pH Changes in RESPIRATORY ALKALOSIS are:
(i) Acute response pH 7.7p7.6 (initial 10 minutes)
(ii) Chronic response pH 7.6p
7.45 (upper normal limit within 8 days)
Gold trunk2. Summary of changes in pH
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Respiratory acidosis Gold trunk
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Respiratory alkalosis Gold trunk
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Respiratory Disturbance of pH
� The disturbances of pH caused byhypoventilation and by hyperventilation areknown as µgaseous¶ or µrespiratory¶
acidosis and alkalosis
� They indicate that the disturbances arise
from mishandling of the blood gases or from an inappropriate rate of pulmonaryventilation
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Compensation in Respiratory Acidosis
� Assisted breathing:
± A respirator is used to assist breathing by
expelling CO2, thus reducing PCO2 in blood
� Bicarbonate is generated and reabsorbed
by renal tubules
� Renal system excretes H+ in urine
� Renal bicarbonate is returned to blood to
bring up pH to normal
Pl ease read
A respirator is a device (alat) to assist (help) a patient to breathe (bernafas).
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Compensatory response in
respiratory acidosis
� Berikut ialah di antara responskompensatori asidosis pernafasan:
A. Hiperventilasi tidak boleh berlaku sebab paru-
paru rosak/tersumbat dan tidak boleh berfungsiB. Peningkatan ventilasi alveolar melalui respirator
mengurangkan PCO2 darah
C. Ion bikarbonat dijana serta diserap semula olehtubul renal
D. Sistem renal meningkatkan perkumuhan H+
dalam urin
E. Lebih banyak ion bikarbonat yang dihasilkan direnal memasuki darah
Pl ease read
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T erms used for describing compensation
� C ompensated ± The compensatory mechanisms have come into play
in a normal manner; does not necessarily imply thatthe plasma pH is within the normal range
� Uncompensated ± Compensation cannot occur due to some
abnormality; patient may show no sign of compensation
� P artiall y compensated ± Intermediate state where compensation is occurring
but is not yet as complete as it should be
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Primary Conditions & Compensation
� Four primary conditions are possible:
1. Respiratory acidosis+ acute blood response
+ chronic renal response
2. Respiratory alkalosis+ acute blood response
+ chronic renal response
3. Metabolic acidosis+ respiratory response
4. Metabolic alkalosis+ respiratory response
S low compensation ( 4 days)
Fast compensation ( 2 4 h)
Fast compensation ( 2 4 h)
R apid compensation (10 min)
S low compensation (8 days)
R apid compensation (10 min)
T wo-phase
process
S ingle-phase
process
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Metabolic and Respiratory Acid-
Base Changes in BloodpH pCO2 HCO3
-
Acidosis
1. Acute metabolic q N q
2. Compensated metabolic N q q3. Acute respiratory q o N
4. Compensated respiratory N o o
Alkalosis
1. Acute metabolic o N o
2. Chronic metabolic o o o
3. Acute respiratory o q N
4. Compensated respiratory N q qq=decreased; o=increased; N=normal
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Compensation in respiratory disorders
� Compensation in respiratory disorders is a two-phase process:
± Acute response: initial 10 minutes
� Involves body buffers
± C hronic (renal) adaptation: for up to 4-8 days
� The change in the bicarbonate level represents the kidney¶sattempt to compensate for the respiratory acidosis or
alkalosis
± pH returns towards normal:
pH 7.7pH 7.6
pH 7.5
pH 7.4
pH 7.3
pH 7.2
pH 7.1 Respiratory acidosisAcute
Chronic
Respiratory alkalosis
Acute
Chronic
4 days8 days
10 min
10 min
Gold trunk
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Compensation in metabolic disorders
� The change in the PCO2 in the metabolic
disorders represents the lung¶s role in
compensation
� Compensation may take up to 1 day (24 hours)
� pH returns towards normal:
pH 7.6
pH 7.5
pH 7.4
pH 7.3
pH 7.2
pH 7.1
pH 7.0
Metabolic acidosis Metabolic alkalosis
24 hr 24 hr
Gold trunk
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Respiratory acidosis Gold trunk
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Respiratory alkalosis Gold trunk
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Compensation in respiratory disorders
1. Compensation in respiratory disorders is a two-phase process
2. Changes in pH occur within 10 minutes, and up to:
(i) 4 days in respiratory acidosis
(ii) 8 days in respiratory alkalosis
3. When partially compensated, pH has still not returned towards normal
4. When fully compensated, pH returns towards normal but not pH 7.4
5. pH Changes in RESPIRATORY ACIDOSIS are:
(i) Acute response pH 7.1p7.2 (initial 10 minutes)
(ii) Chronic response pH 7.2p7.35 (lower normal limit within 4 days)
6. pH Changes in RESPIRATORY ALKALOSIS are:
(i) Acute response pH 7.7p7.6 (initial 10 minutes)
(ii) Chronic response pH 7.6p7.45 (upper normal limit within 8 days)
Gold trunkSummary of changes in pH
Pl d
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Compensation in Respiratory Acidosis
� Assisted breathing:
± A respirator is used to assist breathing by
expelling CO2, thus reducing PCO2 in blood
� Bicarbonate is generated and reabsorbed
by renal tubules
� Renal system excretes H+ in urine
� Renal bicarbonate is returned to blood to
bring up pH to normal
Pl ease read
A respirator is a device (alat) to assist (help) a patient to breathe (bernafas).
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Compensatory response in
respiratory acidosis
� Berikut ialah di antara responskompensatori asidosis pernafasan:
A. Hiperventilasi tidak boleh berlaku sebab paru-
paru rosak/tersumbat dan tidak boleh berfungsiB. Peningkatan ventilasi alveolar melalui respirator
mengurangkan PCO2 darah
C. Ion bikarbonat dijana serta diserap semula olehtubul renal
D. Sistem renal meningkatkan perkumuhan H+
dalam urin
E. Lebih banyak ion bikarbonat yang dihasilkan direnal memasuki darah
Pl ease read
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Patients with Metabolic Acidosis
� Excess acid in blood± removes HCO3
- from the plasma, lowering pH and stimulating
the peripheral chemoreceptors to increase breathing
± lowers P CO2, making the CSF more alkaline, so that the central
chemoreceptors act at first to oppose the respiratory stimulation
± Consequently, the typical hyperventilation that accompanies a
sustained acidosis takes 1 to 2 days to develop, while the
[HCO3-] in the CSF is being reduced
� If the acidosis in the blood is suddenly relieved± the hyperventilation may still continue because the patient is
like the acclimatised mountaineer who has come down quickly
± the [HCO3-] in his CSF is low, and he must continue to
hyperventilate until it rises to normal
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Metabolic Acidosis
[HCO3-]
(mmol/L)
Acid-base Disturbance pH HCO3- PCO2
Metabolic acidosis q q q q
The primary lesion in metabolic acidosis is reduced [HCO3-]
qq [HCO3-]
Normal
Bicarbonate is reduced in metabolic acidosis
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Metabolic Acidosis
PCO2(mmHg)
22.5
Acid-base Disturbance pH HCO3- PCO2
Metabolic acidosis q q q q
pH, HCO3- in same direction; PCO2 will follow HCO3
-
q [PCO2-]
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Metabolic Acidosis
7.25pH
Compensation in METABOLIC ACIDOSIS:
pH returns towards normal (but is never normal)
pH o from pH 7.0p7.25 within 1 day
At full compensation, final pH reaches 7.25 (lower than in respiratory acidosis)
pH Observed During Compensation
(1 day)
pH, HCO3-
in same
direction
Full compensation
Partial compensation
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� The primary lesion in
metabolic acidosis isreduced [HCO3-] from
25p10 mmol/L
� The compensatoryresponse to lowered
plasma bicarbonate isdecreased PCO2 from40p22.5 mmHg
Observe pH o from 7.0p7.25
Acid-base
Disturbance
pH HCO3- PCO2
Metabolic
acidosisq q q q
Comp1rInitial
M t b li id i
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Metabolic acidosis Gold trunk
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Compensation in
Metabolic Acidosis� The primary lesion in
metabolic acidosis isreduced [HCO3
-] from25p10 mmol/L
� The compensatoryresponse to loweredplasma bicarbonate isdecreased PCO2 from
40p
22.5 mmHg
Observe pH o from7.0p7.25
START
BLOOD
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Metabolic Alkalosis
Acid-base Disturbance pH HCO3- PCO2
Metabolic alkalosis o o o o
[HCO3-]
(mmol/L)
The primary lesion in metabolic acidosis is increased [HCO3-
]
oo [HCO3-]
Normal
Bicarbonate is increased in metabolic alkalosis
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Metabolic Alkalosis
50
Acid-base Disturbance pH HCO3- PCO2
Metabolic alkalosis o o o o
PCO2
(mmHg)
pH, HCO3- in same direction; PCO2 will follow HCO3-
o[PCO2
-
]Normal
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Metabolic Alkalosis
pH
Compensation in METABOLIC ALKALOSIS:
pH returns towards normal (but is never normal)
pH q from pH 7.6p7.5 within 1 day
At full compensation, final pH is 7.5 (higher than in respiratory alkalosis)
pH, HCO3-
in same
direction
(1 day)
pH Observed During Compensation
Full compensation
Partial compensation
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� The primary lesion inmetabolic alkalosis isincreased [HCO3
-]
from 25p40 mmol/L
� The compensatoryresponse to elevatedplasma bicarbonate isincreased PCO2 from
40p50 mmHg
� Observe pH q from7.6p7.5
Acid-base
Disturbance
pH HCO3- PCO2
Metabolic
alkalosis o o o o
Comp1rInitial
Metabolic alkalosis
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Metabolic alkalosis Gold trunk
ST
ART
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Compensation in
Metabolic Alkalosis� The primary lesion in
metabolic alkalosis isincreased [HCO3
-] from25p40 mmol/L
� The compensatoryresponse to elevatedplasma bicarbonate isincreased PCO2 from
40p
50 mmHg
� Observe pH q from7.6p7.5
START
BLOOD
Summary of changes in pH
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Compensation in Metabolic Disorders
� The change in the PCO2 in the metabolic disorders represents thelung¶s role in compensation
� Compensation may take up to 1 day (24 hours)
� pH returns towards normal (but is never normal) in metabolic disorders
� pH o in METABOLIC ACIDOSIS from pH 7.0p7.25 within 1 day.
Final pH is lower than in respiratory acidosis
� pH q in METABOLIC ALKALOSIS from pH 7.6p7.5 within 1 day.
Final pH is higher than in respiratory alkalosis
pH 7.6
pH 7.5
pH 7.4
pH 7.3
pH 7.2
pH 7.1
pH 7.0
METABOLIC ACIDOSIS METABOLIC ALKALOSIS
24 hr 24 hr
Gold trunk
pH 7.0p7.25 pH 7.6p7.5
Summary of changes in pH
Summary of changes in PCO2
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Compensation in Metabolic Disorders
� The change in the PCO2 in the metabolic disorders represents thelung¶s role in compensation
� Compensation may take up to 1 day (24 hours)
� pCO2 returns towards normal (but is never normal)?
� pCO2 q in METABOLIC ACIDOSIS from 40p22.5 mmHg within 1 day.
Final pCO2 is lower than in respiratory acidosis
� pCO2 o in METABOLIC ALKALOSIS from 40p50 within 1 day.
Final pCO2 is higher than in respiratory alkalosis
Gold trunkSummary of changes in PCO2
METABOLIC ACIDOSIS METABOLIC ALKALOSIS
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Part 4
� Indicators of hypoxaemia and hypoxia
� Hypercapnia
± Major causes of hypercapnia
± Clinical features of hypercapnia
± Hypoxemia and hypercapnia
� Hypocapnia
± Causes of hypocapnia
± Clinical features of hypocapnia
Own reading
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Indicators of hypoxaemia and hypoxia
Arterial blood gases Lab Findings
PO2
80-100 mm Hg (normal)
60-80 mm Hg (mild hypoxemia)
40-60 mm Hg (moderate hypoxemia)
<40 mm Hg (severe hypoxemia)
SO2
95%-97% (normal)
<90% (may indicate hypoxemia)
pH
7.35-7.45 (normal)
<7.35 (acidemia)
>7.45 (alkalemia)
PCO2
35-45 mm Hg (normal)
>45 mm Hg (hypoventilation)
<35 mm Hg (hyperventilation)
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Indicators of hypoxaemia and hypoxia
System Clinical Signs
Respiratory system Tachypnea, decreased tidal
volume, dyspnea, yawning, use of
accessory respiratory muscles,
flared nostrils
Central nervous system Headache (from cerebral
vasodilation), mental confusion,
bizarre behaviour, restlessness,
agitation, anxious facialexpression, sweating, drowsiness
progressing to coma when hypoxia
is severe
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Hypoxemia and hypercapnia
� By definition, hypoxemia is present in respiratory
failure ± patient may need oxygen support
� Hypoxemic respiratory failure is characterised byhypoxemia and either normocapnia or
hypocapnia
� Ventilatory failure is characterised by hypoxemia
and hypercapnia
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Indicators of hypoxaemia and hypoxia
System Clinical Signs
Cardiovascular system Tachycardia early; bradycardia
later when the heart muscle isnot receiving adequate O2, rise
in BP followed by a drop when
hypoxia remains uncorrected;
dysrhythmiasSkin Cyanosis of lips, oral mucosa,
and nailbeds
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Major causes of hypercapnia
� The major causes of hypercapnia are
obstructive airways disease, respiratory
depressant drugs, weakness or paralysis
of the respiratory muscles, chest trauma or abdominal surgery causing shallow
respirations, and loss of lung tissue ± e.g.,
when diabetic patient lies in bed for toolong, lazy to get up to go to toilet, lazy to
do exercises, silly ideas, uncooperative «
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Clinical features of hypercapnia
� Clinical signs associated with hypercapnia
are mental confusion progressing to coma,
headache (as a result of cerebral
vasodilation), asterixis or flapping tremor of the outstretched hands, and a pulse of
large volume with warm, sweaty
extremities (as a result of the peripheralvasodilation caused by the hypercapnia) ±
as the diabetic patient stretches her hand
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Clinical features of hypercapnia
� In chronic hypercapnia resulting fromchronic pulmonary disease, the patientmay become abnormally tolerant to the
high PCO2, so that the principal drive torespiration is hypoxia
± E.g., the lazy diabetic patient who complaintsof difficulty breathing
± Danger ! Under these circumstances, if O2 isadministered at a high concentration,respiration is diminished and the hypercapniais increased
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Hypocapnia
� Excessive loss of CO2 from the lungs
(hypocapnia) occurs when there is
hyperventilation (ventilation in excess of
metabolic need to remove CO2)
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Causes of hypocapnia
� Common causes of hyperventilation
include brain injury/cerebral trauma,
tumour , aspirin poisoning, anxiety,
compensation for metabolic acidosis/compensatory response to hypoxia, or
excessive mechanical ventilation - asthma
and pneumonia
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Clinical features of hypocapnia
� Signs and symptoms typically associated
with hypocapnia include frequent sighing
and yawning, dizziness, palpitations,
tingling and numbness in the extremeties,and muscular twitches
� Danger ! Severe hypocapnia (PCO2 <25mm Hg) may cause convulsions
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Part 5
� Serum values in acid-base disturbances
� Serum electrolytes values
� Upper limits of arterial blood pH andbicarbonate
� Acid-base map
� Summary of pure acid-base disorders
Own reading
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Serum Values in Acid-Base Disturbances
Condition Na+
mmol/LCl-mmol/L
HCO3-
mmol/LpCO2
mmHgpH
Normal 140 105 25 40 7.40
Metabolic acidosis 140 115 15 31 7.30
Chronic respiratory alkalosis 136 102 25 40 7.44
Mixed metabolic acidosis and
chronic respiratory alkalosis
136 108 14 24 7.39
Metabolic alkalosis 140 92 36 48 7.49
Chronic respiratory acidosis 140 100-102 28 50 7.37
Mixed metabolic alkalosis and
chronic respiratory acidosis
140 90 40 67 7.40
S V l i A id B Di t b
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Serum Values in Acid-Base Disturbances
Condition Na+
mmol/L
Cl-
mmol/L
HCO3-
mmol/L
pCO2
mmHg
pH
Normal 136-145 100-106 24-26 35-45 7.35-7.45
Metabolic alkalosis 139 89q 35o 47o 7.49o
Respiratory alkalosis 136 102 20q 30q 7.44
Mixed alkalosis, mild 139 92q 32o 39 7.53o
Mixed alkalosis, severe 139 92q 32o 30q 7.63o
Mixed chronic respiratory
acidosis and acute
metabolic acidosis
136 102 22q 55o 7.22q
Mixed metabolic acidosis
and metabolic alkalosis
140 103 25 40 7.40
Mi d M t b li A id i d
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Mixed Metabolic Acidosis and
Chronic Respiratory Alkalosis
E xamples:
� Sepsis
� Addition of respiratory alkalosis tometabolic acidosis further decreases
HCO3- but pH may remain normal
� Lactic acidosis plus respiratory alkalosis
due to severe liver disease, pulmonary
emboli, or sepsis
Mi d M t b li Alk l i d
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Mixed Metabolic Alkalosis and
Chronic Respiratory Acidosis
E xamples:
� Patient with COPD receiving
glucocorticoids or diuretics
� pCO2 and HCO3- are increased by both
conditions, but pH is neutralized
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Mixed Alkalosis, Severe
E xample:
� Postoperative patient with severe
hemorrhage stimulating hyperventilation
[respiratory alkalosis] plus massive
transfusion and nasogastric drainage
[metabolic alkalosis]
Mixed Chronic Respiratory Acidosis
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Mixed Chronic Respiratory Acidosis
and Acute Metabolic Acidosis
E xamples:
� COPD [chronic respiratory acidosis] with
severe diarrhoea [metabolic acidosis]. pH
is too low for pCO2 of 55 mmHg in chronic
respiratory acidosis, indicating low pH due
to mixed acidosis, but HCO3- effect is
offset
Mixed Metabolic Acidosis and
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Mixed Metabolic Acidosis and
Metabolic Alkalosis
E xamples:
� Gastroenteritis with vomiting [metabolic
alkalosis] and diarrhoea [metabolic
acidosis due to loss of HCO3-]; surprisingly
normal findings with marked volume
depletion
Serum Electrolyte Values in
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Serum Electrolyte Values in
Various Conditions
ConditionqpH
qHCO3-
mmol/L
K+
mmol/L
Na+
mmol/L
Cl-
mmol/L
Normal 7.35-7.45 24-26 3.5-5.0 136-145 100-106
Metabolic acidosisDiabetic acidosis 7.2 10 5.6o 122q 80q
Fasting 7.2 16 5.2o 142 100
Severe diar hoea 7.2 12 3.2q 128q 96q
Hyperchloremic acidosis 7.2 12 5.2o 142 116o
Addison¶s disease 7.2 22 6.5o 111q 72q
Nephritis 7.2 8 4.0 129q 90q
Nephrosis 7.2 20 5.5o 138 113o
Serum Electrolyte Values in
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Serum Electrolyte Values in
Various Conditions
ConditionpH
HCO3-
mmol/L
K+
mmol/L
Na+
mmol/L
Cl-
mmol/L
Normal 7.35-7.45 24-26 3.5-5.0 136-145 100-106Metabolic alkalosis
Vomiting 7.6o 38o 3.2q 150o 94q
Pyloric obstruction 7.6o 58o 3.2q 132q 42q
Duodenal obstruction 7.6o 42o 3.2q 138 49q
Respiratory acidosis 7.1q 30o 5.5o 142 80q
Respiratory alkalosis 7.6o 14q 5.5o 136 112o
U Li it f A t i l Bl d H d [HCO ]
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Upper Limits of Arterial Blood pH and [HCO3-]
(Expected for Blood pCO2 Values)
Arterial Blood Calculated
HCO3-
mmol/L
pCO2
mmHgpH
20 7.66 22.8
30 7.53 25.6
40 7.57 27.3
60 7.29 27.9
80 7.18 28.9
Values shown are the upper limits of the 95% confidence bands
Source: Coe FL, Metabolic alkalosis. JAMA 1977; 2238-2288
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(Jacques Wallach,
7th edition, 2000;
Fig. 12-1, page
495 - Acid-Base
Map)
What are
normal ABG
values?
Summary of Pure and Mixed Acid
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Summary of Pure and Mixed Acid-
Base Disorders
Decreased pH Normal pH Increased pH
NormalpCO2
Metabolic acidosis Normal Metabolic alkalosis
q pCO2Metabolic acidosis with
incompletely compensated
respiratory alkalosis or
coexisting respiratory
alkalosis
Respiratory
alkalosis and
compensated
metabolic acidosis
Respiratory alkalosis
with or without
incompletely
compensated
metabolic acidosis or
coexisting metabolic
alkalosis
Source: Adapted from Friedman HH. Problem-oriented medical diagnosis, 3rd
ed. Boston: Little, Brown. 1983
Summary of Pure and Mixed Acid
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Summary of Pure and Mixed Acid-
Base Disorders
Decreased
pH
Normal pH Increased
pH
o pCO2Respiratory acidosis
with or without
incompletely
compensated
metabolic alkalosis or
coexisting metabolic
acidosis
Respiratory
acidosis and
compensated
metabolic alkalosis
Metabolic alkalosis
with incompletely
compensated
respiratory acidosis
or coexisting
respiratory acidosis
Normal
pCO2
Metabolic acidosis Normal Metabolic alkalosis
Source: Adapted from Friedman HH. Problem-oriented medical diagnosis, 3rd
ed. Boston: Little, Brown. 1983
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90
Reference
� R enal Block
± R enal compensatory mechanisms in acid-base
imbalance
� Reference:
± Biochemistry: A Comprehensive Review for Medical
Students. Essentials of Modern Biochemistry.
Rudolf Werner
QU4 W494 1983
Pages 339-341
Own reading
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91
Reference
� An illustrated colour text. Clinical
Biochemistry.
Allan Gaw, Robert A. Cowan, Denis St. J.
O¶Reilly, Michael J. Stewart, JamesShepherd
Churchill Livingstone, London
1995, pages 34-43RM45 (Syarikat Kamal)
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92
Reference
� Interpretation of Diagnostic Tests
Jacques Wallach
Seventh Edition, 2000
Lippincott Williams & Wilkins, Philadelphia
Chapter 12 ± Acid-Base Disorders, pages
489-500
RM100 (Syarikat Kamal)
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93
Reference
� Clinical Chemistry in Diagnosis and Treatment.
Philip D. Mayne
Sixth edition, 1994
Educational Low-Priced Books Scheme funded bythe British Government
RM15 (Koperasi UNIKEB)
Chapter 4
Hydrogen ion homeostasis, pages 79-90Disturbances of hydrogen ion homeostasis, pages 90-104
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94
Reference
� A Primer of Chemical Pathology.1996± Evelyn S.C. Koay
± Noel Walmsley
� World ScientificPublishing Co. Pte. Ltd.
� Singapore
� QY4 K75 1996
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95
S tudy guide
Acid-base:
� Identify the primary disorder (lesion)
� List possible causes
� Describe the causative mechanism
� Describe the compensatory mechanism
� Determine the level of compensation
Own reading
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Acid-base algorithms
� Online resources:
± Cecil Textbook of Medicine
± Harrison¶s Principles of Internal Medicine
± Current Medical Diagnosis & Treatment
± www.amazon.com
± www.google.com
Own reading
Type acid-base
in the search box