Respiratory Mechanisms in Acid-Base Homeostasis Yr1 MD 26Feb2005

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Respiratory Mechanisms

in Acid - Base Homeostasis

Assoc. Prof. Faridah Abdul RashidDept. of Chemical Pathology

School of Medical SciencesUSM Kubang Kerian, Kelantan

[email protected]

Medicine 2004/2005

Phase 1, Year 1

Respiratory Block, Week 2

Saturday, 26 February 2005, 8:30 am ± 9:30 am, DK4



2

Part 1

� Normal values for arterial blood gases

� Carbonic acid/bicarbonate buffer system

� Henderson-Hasselbalch equation

Own reading



3

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



4

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



5

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:



6

� 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



7

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



8

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



9

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



10

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



11

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



12

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



13

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



14

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



15

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



16

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



18

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



19

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



20

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



21

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



22

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



23

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



24

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



25

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)



26

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



27

Memorise

Acid-base changes in acidosis and alkalosis


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



28

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



29

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.



30

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.



31

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



32


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



33


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



34


1. Compensation in respiratory disorders is a two-phase process


(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



35

Respiratory acidosis Gold trunk



36

Respiratory alkalosis Gold trunk



37

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



38

Compensation in Respiratory Acidosis


± 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).



39

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



40

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



41

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



42

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



43


� 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



44

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



45

Respiratory acidosis Gold trunk



46

Respiratory alkalosis Gold trunk



47


1. Compensation in respiratory disorders is a two-phase process


(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:


(ii) Chronic response pH 7.2p7.35 (lower normal limit within 4 days)

6. pH Changes in RESPIRATORY ALKALOSIS are:


(ii) Chronic response pH 7.6p7.45 (upper normal limit within 8 days)

Gold trunkSummary of changes in pH

Pl d



48

Compensation in Respiratory Acidosis


± 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).



49

Compensatory response in


� 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



50

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



51

Metabolic Acidosis

[HCO3-]

(mmol/L)


Metabolic acidosis q q q q

The primary lesion in metabolic acidosis is reduced [HCO3-]

qq [HCO3-]

Normal

Bicarbonate is reduced in metabolic acidosis



52

Metabolic Acidosis

PCO2(mmHg)

22.5


Metabolic acidosis q q q q

pH, HCO3- in same direction; PCO2 will follow HCO3

-

q [PCO2-]



53

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



54

� 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



55

Metabolic acidosis Gold trunk



56

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



57

Metabolic Alkalosis


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



58

Metabolic Alkalosis

50


Metabolic alkalosis o o o o

PCO2

(mmHg)

pH, HCO3- in same direction; PCO2 will follow HCO3-

o[PCO2

-

]Normal



59

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



60

� 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



61

Metabolic alkalosis Gold trunk

ST

ART



62

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



63

Compensation in Metabolic Disorders

� The change in the PCO2 in the metabolic disorders represents thelung¶s role in compensation


� 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



64

Compensation in Metabolic Disorders

� The change in the PCO2 in the metabolic disorders represents thelung¶s role in compensation


� 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



65

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



66

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)



67


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



68

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



69


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



70

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 «



71

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



72

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



73

Hypocapnia

� Excessive loss of CO2 from the lungs

(hypocapnia) occurs when there is

hyperventilation (ventilation in excess of

metabolic need to remove CO2)



74

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



75

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



76

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



77

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



78

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



79

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



80

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



81

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



82

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




83


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



84


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




85


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 ]



86

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



87

(Jacques Wallach,

7th edition, 2000;

Fig. 12-1, page

495 - Acid-Base

Map)

What are

normal ABG

values?

Summary of Pure and Mixed Acid



88

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



89

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


or coexisting


Normal

pCO2

Metabolic acidosis Normal Metabolic alkalosis

Source: Adapted from Friedman HH. Problem-oriented medical diagnosis, 3rd

ed. Boston: Little, Brown. 1983



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



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)



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)



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



94

Reference

� A Primer of Chemical Pathology.1996± Evelyn S.C. Koay

± Noel Walmsley

� World ScientificPublishing Co. Pte. Ltd.

� Singapore

� QY4 K75 1996



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



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

Respiratory Mechanisms in Acid-Base Homeostasis Yr1 MD 26Feb2005

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