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. Shock), heart failure (Chap. 124. Heart Failure and Cor Pulmonale), and peripheral vascular disease (Chap. 126. Peripheral Vascular Disease) with arterial obstruction or vasospasm (Table 34-1). 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).
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For a more detailed discussion, see Loscalzo J: Hypoxia and Cyanosis, Chap. 49, p. 247, in HPIM-19. |