Bluish discoloration of the skin and/or mucous membranes are usually due to elevated quantity of reduced hemoglobin (>40 g/L [>4 g/dL]) in the capillary blood vessels. Findings are most apparent in the lips, nail beds, ears, and malar eminences.
Results from arterial desaturation or presence of an abnormal hemoglobin. Usually evident when arterial saturation is ≤85%, or ≤75% in dark-skinned individuals. Etiologies include:
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, secondary polycythemia is often present.
Anatomic vascular shunting: Shunting of desaturated venous blood into the arterial circulation may result from congenital heart disease or pulmonary atrioventricular (AV) fistula.
Decreased inspired O2: Cyanosis may develop in ascents to altitudes >4000 m (>13,000 ft).
Abnormal hemoglobins: Methemoglobinemia, sulfhemoglobinemia, and mutant hemoglobins with low oxygen affinity (see Chap. 127, HPIM-19).
Occurs with normal arterial O2 saturation with increased extraction of O2 from capillary blood caused by decreased localized blood flow. Contributors include vasoconstriction due to cold exposure, decreased cardiac output (e.g., in shock, Chap. 11), heart failure (Chap. 124), and peripheral vascular disease (Chap. 126) with arterial obstruction or vasospasm (Table 34-1). Local (e.g., thrombophlebitis) or central (e.g., constrictive pericarditis) venous hypertension intensifies cyanosis.
TABLE 34-1CAUSES OF CYANOSIS |Favorite Table|Download (.pdf) TABLE 34-1CAUSES OF CYANOSIS
|Central Cyanosis |
|Decreased arterial oxygen saturation |
| Decreased atmospheric pressure—high altitude |
| Impaired pulmonary function |
| Alveolar hypoventilation |
| Inhomogeneity in pulmonary ventilation and perfusion (perfusion of hypoventilated alveoli) |
| Impaired oxygen diffusion |
|Anatomic shunts |
| Certain types of congenital heart disease |
| Pulmonary arteriovenous fistulas |
| Multiple small intrapulmonary shunts |
| Hemoglobin with low affinity for oxygen |
|Hemoglobin abnormalities |
| Methemoglobinemia—hereditary, acquired |
| Sulfhemoglobinemia—acquired |
| Carboxyhemoglobinemia (not true cyanosis) |
|Peripheral Cyanosis |
|Reduced cardiac output |
|Cold exposure |
|Redistribution of blood flow from extremities |
|Arterial obstruction |
|Venous obstruction |
APPROACH TO THE PATIENT: Cyanosis
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 is most intense in nailbeds and may resolve with gentle warming of extremities.
Check for clubbing, i.e., selective enlargement of the distal segments of fingers and toes, due to proliferation of connective tissue. Clubbing may be hereditary, idiopathic, or acquired in association with lung cancer, infective endocarditis, bronchiectasis, or hepatic cirrhosis. Combination of clubbing and cyanosis is frequent in congenital heart disease and occasionally in 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.