Cyanosis

[Section Outline]

Central Cyanosis
Peripheral Cyanosis

Bluish discoloration of the skin and/or mucous membranes are usually due to elevated quantity of reduced hemoglobin (>4 g/dL) in the capillary blood vessels. Findings are most apparent in the lips, nail beds, ears, and malar eminences. Cyanosis depends on absolute, not relative, quantity of desaturated hemoglobin, so may be less evident in pts with severe anemia, and more notable in pts with polycythemia.

Central Cyanosis

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 (see Chap. 94, HPIM-20).

Peripheral Cyanosis

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. 12 Shock), heart failure (Chap. 126 Heart Failure and Cor Pulmonale), and peripheral vascular disease (Chap. 128 Peripheral Vascular Disease) with arterial obstruction or vasospasm (Table 36-1 Causes of Cyanosis). Local (e.g., thrombophlebitis) or central (e.g., constrictive pericarditis) venous hypertension intensifies cyanosis.

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. 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 for abnormal hemoglobins (e.g., spectroscopy, measurement of methemoglobin level).