Harrison’s Manual of Medicine
The circulating quantity of reduced hemoglobin is elevated [>50 g/L (>5 g/ dL)] resulting in bluish discoloration of the skin and/or mucous membranes.
Results from arterial desaturation. Usually evident when arterial saturation is £85%. Particularly in dark-skinned individuals, cyanosis may not be detected until saturation is 75%.
1. Impaired pulmonary function: Poorly ventilated alveoli or impaired oxygen diffusion; most frequent in pneumonia, pulmonary edema, and chronic obstructive pulmonary disease (COPD); in COPD with cyanosis, polycythemia is often present.
2. Anatomic vascular shunting: Shunting of desaturated venous blood into the arterial circulation may result from congenital heart disease or pulmonary AV fistula.
3. Decreased inspired O2: Cyanosis may develop in ascents to altitudes >2400 m (>8000 ft).
4. Abnormal hemoglobins: Methemoglobinemia, sulfhemoglobinemia, and mutant hemoglobins with low oxygen affinity (see HPIM-15, Chap. 106).
Occurs with normal arterial O2 saturation with increased extraction of O2 from capillary blood caused by decreased localized blood flow. Vasoconstriction due to cold exposure, decreased cardiac output (in shock, Chap. 30), and peripheral vascular disease (Chap. 126) with arterial obstruction or vasospasm (Table 16-1). Local (e.g., thrombophlebitis) or central (e.g., constrictive pericarditis) venous hypertension intensifies cyanosis.
Table 16-1 Causes of Cyanosis
Approach to the Patient
Inquire about duration (cyanosis since birth suggests congenital heart disease) and exposures (drugs or chemicals that result in abnormal hemoglobins).
Differentiate central from peripheral cyanosis by examining nailbeds, lips, and mucous membranes. Peripheral cyanosis may resolve with gentle warming of extremities.
Check for clubbing of fingers and toes; clubbing is the selective enlargement of the distal segments of fingers and toes. Clubbing may be hereditary, idiopathic, or acquired and is associated with a variety of disorders. Combination of clubbing and cyanosis is frequent in congenital heart disease and occasionally with pulmonary disease (lung abscess, pulmonary AV shunts but not with uncomplicated obstructive lung disease).
Examine chest for evidence of pulmonary disease, pulmonary edema, or murmurs associated with congenital heart disease.
If cyanosis is localized to an extremity, evaluate for peripheral vascular obstruction.
Obtain arterial blood gas to measure systemic O2 saturation. Repeat while pt inhales 100% O2; if saturation fails to increase to >95%, intravascular shunting of blood bypassing the lungs is likely (e.g., right-to-left intracardiac shunts).
Evaluate abnormal hemoglobins by hemoglobin electrophoresis and measurement of methemoglobin level.
For a more detailed discussion, see Braunwald E: Hypoxia and Cyanosis, Chap. 36, p. 214, in HPIM-15.