Cyanosis is a bluish discoloration of the skin or mucous membranes due to excessive amounts of deoxygenated hemoglobin. It can be central or peripheral in origin. Central cyanosis occurs when oxygen saturation in arterial blood is low, such as in congenital heart defects causing right-to-left shunts. Peripheral cyanosis is caused by slowed blood flow and high oxygen extraction from normally saturated blood, as seen in cold exposure, shock, or peripheral vascular disease. Differential cyanosis may present with cyanosis isolated to certain limbs depending on anatomy. Methemoglobinemia and sulfhemoglobinemia can also cause cyanosis and require specific treatments.

1. CYANOSIS
Dr.G.VENKATA RAMANA
MBBS DNB FAMILY MEDICINE

2. • Bluish color of the skin and mucous membranes
resulting from an increased quantity of reduced
hemoglobin (i.e., deoxygenated hemoglobin) or
of hemoglobin derivatives (e.g., methemoglobin
or sulfhemoglobin) in the small blood vessels of
those tissues
• It is usually most marked in the lips, nail beds,
ears, and malar eminences
• Types
• Central
• Peripheral
• Differential

3. • The increase in the quantity of reduced hemoglobin in
the mucocutaneous vessels that produces cyanosis may
be brought about either by an increase in the quantity of
venous blood as a result of dilation of the venules
(including precapillary venules) or by a reduction in the
Sao2 in the capillary blood
• In general, cyanosis becomes apparent when the
concentration of reduced hemoglobin in capillary blood
exceeds 40 g/L (4 g/dL)
• It is the absolute, rather than the relative, quantity of
reduced hemoglobin that is important in producing
cyanosis
• Thus, in a patient with severe anemia, the relative
quantity of reduced hemoglobin in the venous blood may
be very large when considered in relation to the total
quantity of hemoglobin in the blood

4. • However, since the concentration of the latter is
markedly reduced, the absolute quantity of reduced
hemoglobin may still be low, and, therefore, patients with
severe anemia and even marked arterial desaturation
may not display cyanosis
• Conversely, the higher the total hemoglobin content, the
greater is the tendency toward cyanosis; thus, patients
with marked polycythemia tend to be cyanotic at higher
levels of Sao2 than patients with normal hematocrit
values
• Likewise, local passive congestion, which causes an
increase in the total quantity of reduced hemoglobin in
the vessels in a given area, may cause cyanosis

5. • The degree of cyanosis is modified by the color of
the cutaneous pigment and the thickness of the
skin, as well as by the state of the cutaneous
capillaries
• In some instances, central cyanosis can be
detected reliably when the Sao2 has fallen to 85%;
in others, particularly in dark-skinned persons,it
may not be detected until it has declined to 75%
• In the latter case, examination of the mucous
membranes in the oral cavity and the
conjunctivae rather than examination of the skin
is more helpful in the detection of cyanosis

7. • In central cyanosis, the Sao2 is reduced or an abnormal
hemoglobin derivative is present, and the mucous
membranes and skin are both affected
• Peripheral cyanosis is due to a slowing of blood flow
and abnormally great extraction of O2 from normally
saturated arterial blood
• It results from vasoconstriction and diminished
peripheral blood flow, such as occurs in cold exposure,
shock, congestive failure, and peripheral vascular
disease
• Often in these conditions, the mucous membranes of
the oral cavity, including the sublingual mucosa, may be
spared
• Clinical differentiation between central and peripheral
cyanosis may not always be straightforward, and in
conditions such as cardiogenic shock with pulmonary
edema, there may be a mixture of both types

8. • Central Cyanosis
• Decreased Sao2 results from a marked reduction in the
Pao2
• This reduction may be brought about by a decline in the
Fio2 without sufficient compensatory alveolar
hyperventilation to maintain alveolar Po2
• Cyanosis usually becomes manifest in an ascent to an
altitude of 4000 m (13,000 ft)
• Seriously impaired pulmonary function, through
perfusion of unventilated or poorly ventilated areas of the
lung or alveolar hypoventilation, is a common cause of
central cyanosis
• This condition may occur acutely, as in extensive
pneumonia or pulmonary edema, or chronically, with
chronic pulmonary diseases (e.g., emphysema)
• In the latter situation, secondary polycythemia is
generally present and clubbing of the fingers may occur

9. • Another cause of reduced Sao2 is shunting of systemic
venous blood into the arterial circuit
• Certain forms of congenital heart disease are associated
with cyanosis on this basis
• Pulmonary arteriovenous fistulae may be congenital or
acquired, solitary or multiple, and microscopic or massive
• The severity of cyanosis produced by these fistulae
depends on their size and number
• They occur with some frequency in hereditary hemorrhagic
telangiectasia
• Sao2 reduction and cyanosis may also occur in some
patients with cirrhosis, presumably as a consequence of
pulmonary arteriovenous fistulae or portal vein–pulmonary
vein anastomoses

10. • In patients with cardiac or pulmonary right-to-left shunts, the
presence and severity of cyanosis depend on the size of the
shunt relative to the systemic flow and on the Hb-O2 saturation
of the venous blood.
• With increased extraction of O2 from the blood by the
exercising muscles, the venous blood returning to the right
side of the heart is more unsaturated than at rest, and
shunting of this blood intensifies the cyanosis
• Secondary polycythemia occurs frequently in patients in this
setting and contributes to the cyanosis
• Cyanosis can be caused by small quantities of circulating
methemoglobin (Hb Fe3+) and by even smaller quantities of
sulfhemoglobin
• Both of these hemoglobin derivatives impair oxygen delivery
to the tissues
• Although they are uncommon causes of cyanosis, these
abnormal hemoglobin species should be sought by
spectroscopy when cyanosis is not readily explained by
malfunction of the circulatory or respiratory systems
• Generally, digital clubbing does not occur with them

12. • Peripheral Cyanosis
• Most common cause - Normal vasoconstriction
resulting from exposure to cold air or water
• Site : Nail bed, nose tip, earlobe, extremities
• When cardiac output is reduced, cutaneous
vasoconstriction occurs as a compensatory mechanism
so that blood is diverted from the skin to more vital
areas such as the CNS and heart, and cyanosis of the
extremities may result even though the arterial blood is
normally saturated
• Arterial obstruction to an extremity, as with an embolus,
or arteriolar constriction, as in cold-induced vasospasm
(Raynaud’s phenomenon), generally results in pallor
and coldness, and there may be associated cyanosis
• Venous obstruction, as in thrombophlebitis or deep
venous thrombosis, dilates the subpapillary venous
plexuses and thereby intensifies cyanosis

13. Peripheral cyanosis

16. Differential Cyanosis
• Cyanosis is seen only in the lower limbs - Patent
ductus arteriosus with pulmonary
hypertension,with right to left shunt
• Cyanosis is seen only in the upper limbs - Patent
ductus arteriosus with pulmonary hypertension,
with right to left shunt and transposition of great
vessels
• Rarely, in addition to the lower limbs, the left
upper limb may also be cyanosed when the
patent ductus opens proximal to the origin of left
subclavian artery

17. Methemoglobin Sulfhemoglobin
Common causes Ingested medication (dapsone,
antimalarial agents)
Local anesthetic
Nitrates or nitrites
Ingested medication
(dapsone, phenacetin,
sulfonamides)
Nitrites
Typical
presentation
Cyanosis
Neurologic symptoms from
headache to coma
Respiratory depression
Cyanosis
Color of the blood Chocolate brown Green
Pulse oximetry Inaccurate Inaccurate
Arterial blood gas PaO2 normal
Methemoglobin is detected on
most machines
PaO2 normal
Confirmatory
testing
Blood gas (arterial or venous) Spectrophotometry or
Gas chromatography
Management Methylene blue (MB) or
Ascorbic acid
Supportive (no antidote)
Exchange transfusion in
severe cases
Lack of response to MB

18. Carboxyhemoglobin
Common causes Inhaled CO gas from fires, gas-powered
generators, kerosene heaters
Smoking
Typical presentation Neurologic symptoms from headache to coma
Chest pain from myocardial ischemia
Headache, malaise
Color of the blood Cherry red
Pulse oximetry Inaccurate
Arterial blood gas PaO2 normal
Carboxyhemoglobin is detected on most
machines
Confirmatory testing Co-oximetry using arterial blood (in stable
patients, venous samples are accurate)
Management High-flow or hyperbaric oxygen

19. • There are two types of cyanosis – Iron-replete and iron-
deplete
• Iron-replete compensated erythrocytosis establish equilibrium
with haematocrits and rarely result in symptoms of hyper-
viscosity because iron-replete cells are deformable
• Iron-deplete cells are less deformable and the
decompensated erythrocytosis fails to establish equilibrium
with unstable, rising haematocrits, resulting in recurrent
hyper-viscosity symptoms
• Phelebotomy for symptoms of hyper-viscosity which is not
due to dehydration or iron deficiency is a simple outpatient
procedure involving removal of 500 ml of blood over 45
minutes with isovolumetric replacement of isotonic saline
• Iron repletion in iron-deplete cyanosis must be done gradually

20. • Certain features are important in arriving at
the cause of cyanosis
• History Age,Family disease history, Exposure
to drugs
• 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

22. LAB TESTS
• CBC
• CHEST XRAY
• ECG
• 2DECHO
• ABG
• OXIMETRIC STUDIES
• SPECTROSCOPE
• HB ELECTROPHORESIS