Cyanosis Cyanosis refers to a bluish color of the skin and mucous membranes resulting from an increased quantity of reduced hemoglobin/deoxyhemoglobin or abnormal hemoglobin derivatives, in the small blood vessels of those areas.

1. Cyanosis

2. Definition
Cyanosis refers to a bluish color of the skin
and mucous membranes resulting from
an increased quantity of reduced
hemoglobin/deoxyhemoglobin or
abnormal hemoglobin derivatives, in the
small blood vessels of those areas.

3. Mechanism of Cyanosis
• Absolute increase of amount of reduced
hemoglobin in blood, > 50g/L (capillary)
• Nonfunctional hemoglobin such as
methemoglobinor sulfhemoglobin is
present in blood.

4. reduced hemoglobin in blood
desaturation of oxygen
• Arterial desaturation of oxygen:5%
• Venous desaturation of oxygen:30%
• Capillary desaturation of oxygen:average of both
• SaO2:66% reduced Hb 50g/L

5. Mean capillary concentration of reduced
hemoglobin exceeds 50 g/L. It is the
absolute rather than the relative
increase.

6. 15
5
20
5 5 5
0
5
10
15
20
Total Hb
R-Hb
Normal Polycythemia Anemia
g/dl
Mechanisms of Cyanosis
Caused by absolute increase of amount of reduced
Hb in blood, usually > 5g/dl (capillary)
The higher the hemoglobin concentration,
The greater tendency toward cyanosis.

7. severe anemia
• the relative amount of reduced hemoglobin
in the venous blood may be very large
• the absolute quantity of reduced
hemoglobin may still be small

8. polycythemia
• patients with marked polycythemia tend to
be cyanotic at higher levels of SaO2 than
patients with normal hematocrit

9. Clinical Classification & Etiology
• True Cyanosis (increased amount of reduced Hb)
— Central Type
— Peripheral Type
— Mixed Type
• Cyanosis due to abnormal Hb derivatives
— Methemoglobinemia
— Sulfhemoglobinemia

10. Central cyanosis is caused by decreased
SaO2(increased amount of reduced Hb)

11. Central cyanosis only occurs when the oxygen
saturation of arterial blood is less than 85%.

12. Cause of decreased SaO2
• Parenchymal lung disease
• Right to left cardiac shunt - congenital
cyanotic heart disease
• Decreased PO2 of inspired air - high altitude
• Hypoventilation

13. Parenchymal lung disease
• Airway obstruction,pneumonia,massive pulmonary
embolism, pulmonary edema ,chronic airflow
obstruction emphysema
• Seriously impaired pulmonary function, through
perfusion of unventilated or poorly ventilated areas
of the lung or alveolar hypoventilation,resulting in
decresed alveolar PO2 and SaO2

14. • Congenital cardiac lesion : tetralogy of Fallot (the
combination of ventricular septal defect and
pulmonary outflow tract obstruction ).
• Pulmonary arteriovenous fistulae :congenital or
acquired, solitary or multiple, microscopic or
massive.
Shunting of systemic venous blood into the
arterial circuit
the presence and severity of cyanosis
depend on the size of the shunt relative to the systemic flow as
well as on the Hb-O2 saturation of the venous blood.

16. Impaired pulmonary
function
1. Airway obstruction
2. Pulmonary diseases
Right-to-left shunting
of blood
Tetralogy of Fallot
Central Cyanosis

17. • At 2500 m the FIO2 is about 120 mmHg, the
alveolar PO2 is approximately 80 mmHg, and the
SaO2 is nearly normal
• At 3500 m the FIO2 and alveolar PO2 are about 85
and 50 mmHg, respectively, and the SaO2 is only
about 75%.
• Cyanosis is marked in a further ascent to 3500 m.
The reason :the S shape of the Hb-O2 dissociation
curve.
Decreased PO2 of inspired air

18. High O2
affinity Hgb
normal
Low O2
affinity Hgb

19. Peripheral cyanosis is due to poor peripheral
circulation and increased oxygen consumption in
peripheral tissue.

20. Peripheral Cyanosis
Caused by increased oxygen consumption in
peripheral tissue.
Vasoconstriction
Low cardiac output
Exposure to cold air or water
Slowing of blood flow
Right heart failure

21. Peripheral cyanosis
• Congestive peripheral cyanosis
right-side heart failure, constrictive pericarditis, local venous diseases.
 slowing of blood flow
 abnormally great extraction of O2 from normally saturated arterial
blood.
• Ischmic peripheral cyanosis.
Ischemic peripheral cyanosis is often seen in severe shock.
Arterial obstruction or constriction.
 vasoconstriction and diminished peripheral blood flow

22. Mixed Cyanosis
Clinical differentiation between central and
peripheral cyanosis may not always be
simple, and in conditions such as
cardiogenic shock with pulmonary edema
there may be a mixture of both types.

23. Possible causes of mixed cyanosis
• all causes of central cyanosis may
lead to peripheral cyanosis
• low cardiac output e.g. heart failure

24. Cyanosis due to abnormal Hb derivatives
Central cyanosis may be simulated by
methaemoglobulinaemia and
sulphaemoglobulinaemia.

25. Methemoglobinemia
• Hereditary: very rare
• Acquired: >30g/L in blood
- intake or exposure to some drugs or
chemicals, such as sulfa drugs, nitrite
salt. “ enterogenic cyanosis ”
Spectroscope is helpful to diagnose
methemoglobinemia.

26. Sulfhemoglobinemia
• Sulfhemoglobin >5g/L
• Caused by some drugs or chemicals,
• Spectroscope is helpful to diagnose

27. Clinical Classification
— Central Type
— Peripheral Type
— Mixed Type

28. Possible clinical features include
----central cyanosis
• the warm mucous membranes are blue, for
example the tongue, the inside of the lips
• central cyanosis increases immediately on
exercise which is not the case for peripheral
cyanosis
• there is polycythaemia with an abnormally
high haemoglobin and haematocrit
• clubbing is often seen in patients with
central cyanosis

29. Possible clinical features include
----peripheral cyanosis
• Cool skin and mucous membrance
• Site (lower extremities,fingers)
• Diminish after massage

30. Note that the absolute
discriminating feature between
central and peripheral cyanosis is
obtained from testing the oxygen
saturation of arterial blood.

31. Differentiation of central as opposed to
peripheral
Cyanosis Skin temp. Massage or warming
Central Warm No change
Peripheral Cool Cyanosis fades

32. Possible clinical features include
----abnormal hemoglobin
Acquired Methemoglobinemia
• Acutely develop after intaking drugs or chemicals
(often severe)
• Not relieved after oxygen therapy
• Blood remains brown after being mixed and
exposed to air
• Fades after infusion of methylene blue or
administration of large dosage of vitamin C

33. Sulfhemoglobin
• Long duration(several months)
• Spectroscope-630nm

34. Certain features are important in arriving at
the cause of cyanosis
• History (age, gender, family disease history)
• Clinical differentiation of central as opposed to
peripheral cyanosis
• The presence or absence of clubbing of the digits
• Determination of PaO2 tension and SaO2
• Spectroscopic and other examinations of the blood
for abnormal types of hemoglobin (critical in the
differential diagnosis of cyanosis)

35. History
• particularly the onset (cyanosis present
since birth is usually due to congenital heart
disease)
• possible exposure to drugs or chemicals that
may produce abnormal types of hemoglobin

36. Lab tests
• Determination of arterial oxygen saturation
• Oximetric studies
• physical or radiographic examination ,
echocardiography right heart catherixation and
angiocardiography
• Spectroscope

37. • The combination of cyanosis and clubbing is
frequent in patients with congenital heart disease
and right-to-left shunting and is seen occasionally
in persons with pulmonary disease such as lung
abscess or pulmonary arteriovenous fistulae.
• In contrast, peripheral cyanosis or acutely
developing central cyanosis is not associated with
clubbed digits
Clubbing

38. • Cyanosis + Dyspnea
Disorders of respiratory or cardiovascular system
• Cyanosis with mild or no dyspnea
Methemoglobinemia
Sulfhemoglobinemia: Spectroscopy helpful
• Cyanosis + clubbing
Severe, long duration

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