Cyanosis
Cyanosis — a bluish or bluish black discoloration of the skin and mucous membranes — results from excessive concentration of unoxygenated hemoglobin in the blood. This common sign may develop abruptly or gradually. It can be classified as central or peripheral, although the two types may coexist.
Central cyanosis reflects inadequate oxygenation of systemic arterial blood caused by right-to-left cardiac shunting, pulmonary disease, or hematologic disorders. It may occur anywhere on the skin and also on the mucous membranes of the mouth, lips, and conjunctiva.
Peripheral cyanosis reflects sluggish peripheral circulation caused by vasoconstriction, reduced cardiac output, or vascular occlusion. It may be widespread or may occur locally in one extremity; however, it doesn’t affect mucous membranes. Typically, peripheral cyanosis appears on exposed areas, such as the fingers, nail beds, feet, nose, and ears.
Although cyanosis is an important sign of cardiovascular and pulmonary disorders, it isn’t always an accurate gauge of oxygenation. Several factors contribute to its development: hemoglobin concentration and oxygen saturation (Sao2), cardiac output, and partial pressure of arterial oxygen (Pao2). Cyanosis is usually undetectable until the Sao2 of hemoglobin falls below 80%. Severe cyanosis is quite obvious, whereas mild cyanosis is more difficult to detect, even in natural, bright light. In dark-skinned patients, cyanosis is most apparent in the mucous membranes and nail beds.
Transient, nonpathologic cyanosis may result from environmental factors. For example, peripheral cyanosis may result from cutaneous vasoconstriction following a brief exposure to cold air or water. Central cyanosis may result from reduced Pao2 at high altitudes.
Act Now: If the patient displays sudden, localized cyanosis and other signs of arterial occlusion, protect the affected limb from injury; however, don’t massage the limb. If you see central cyanosis stemming from a pulmonary disorder or shock, perform a rapid evaluation. Take immediate steps to maintain a patent airway, assist breathing, and monitor circulation.
Assessment
History
Ask the patient about cardiac, pulmonary, and hematologic disorders or previous surgeries. Ask whether he’s experiencing chest pain; if so, ask him to rate its severity using a standardized pain rating scale. Note precipitating, aggravating, or alleviating factors and whether the pain radiates. Determine when the patient first noticed the cyanosis and precipitating, aggravating, or alleviating factors; ask whether it’s intermittent or constant. Does the patient have a history of headaches, dizziness, blurred vision, or pain or abnormal sensations in the extremities ? Does he have a cough and if so, is it productive? Ask him to describe sputum. Inquire about a history of sleep apnea. Document the patient’s medication history, including over-the-counter medications.
Physical examination
Obtain the patient’s vital signs. Inspect the skin and mucous membranes to determine the extent of cyanosis. Assess the skin for coolness, pallor, redness, pain, and ulceration. Note the presence of clubbing.
Evaluate the patient’s level of consciousness and test motor strength. Palpate peripheral pulses and test capillary refill time. Auscultate heart rate and rhythm, especially noting gallops and murmurs. Auscultate the abdominal aorta and femoral arteries to detect bruits.
Evaluate respiratory rate and rhythm. Check for nasal flaring and accessory muscle use. Inspect the patient for asymmetrical chest expansion or barrel chest. Percuss the lungs for dullness or hyperresonance, and auscultate for decreased or adventitious breath sounds.
Inspect the abdomen for ascites, and test for shifting dullness or fluid wave. Percuss and palpate for liver enlargement and tenderness.
Pediatric pointers
Many pulmonary disorders responsible for cyanosis in adults also cause cyanosis in children. In addition, central cyanosis may result from cystic fibrosis, asthma, airway obstruction by a foreign body, acute laryngotracheobronchitis, or epiglottiditis. It may also result from a congenital heart defect, such as transposition of the great vessels, that causes right-to-left intracardiac shunting.
In children, circumoral cyanosis may precede generalized cyanosis. Acrocyanosis (also called “glove and bootee” cyanosis) may occur in infants because of excessive crying or exposure to cold. Exercise and agitation enhance cyanosis, so provide comfort and regular rest periods. Also, administer supplemental oxygen during cyanotic episodes.
Geriatric pointers
Because elderly patients have reduced tissue perfusion, peripheral cyanosis can present even with a slight decrease in cardiac output or systemic blood pressure.
Medical causes
With arteriosclerotic occlusive disease, peripheral cyanosis occurs in the legs whenever they’re in a dependent position. Associated signs and symptoms include intermittent claudication and burning pain at rest, paresthesia, pallor, muscle atrophy, weak leg pulses, and impotence. Late signs are leg ulcers and gangrene.
Bronchiectasis produces chronic central cyanosis. Its classic sign, however, is chronic productive cough with copious, foul-smelling, mucopurulent sputum or hemoptysis. Auscultation reveals rhonchi and coarse crackles during inspiration. Other signs and symptoms include dyspnea, recurrent fever and chills, weight loss, malaise, clubbing, and signs of anemia.
With Buerger’s disease, exposure to cold initially causes the feet to become cold, cyanotic, and numb; later, they redden, become hot, and tingle. Intermittent claudication of the instep is characteristic; it’s aggravated by exercise and smoking and relieved by rest. Associated signs and symptoms include weak peripheral pulses and, in later stages, ulceration, muscle atrophy, and gangrene.
Chronic obstructive pulmonary disease (COPD).
Chronic central cyanosis occurs in advanced stages of COPD and may be aggravated by exertion. Associated signs and symptoms include exertional dyspnea, productive cough with thick sputum, anorexia, weight loss, pursed-lip breathing, tachypnea, and accessory muscle use. Examination reveals wheezing and hyperresonant lung fields. Barrel chest and clubbing are late signs. Tachycardia, diaphoresis, and flushing may also accompany COPD.
With deep vein thrombosis, acute peripheral cyanosis occurs in the affected extremity associated with tenderness, painful movement, edema, warmth, and prominent superficial veins. Homans’sign can also be elicited.
Acute or chronic cyanosis may occur in patients with heart failure. Typically, it’s a late sign and may be central, peripheral, or both. With left-sided heart failure, central cyanosis occurs with tachycardia, fatigue, dyspnea, cold intolerance, orthopnea, cough, ventricular or atrial gallop, bibasilar crackles, and diffuse apical impulse. With right-sided heart failure, peripheral cyanosis occurs with fatigue, peripheral edema, ascites, jugular vein distention, and hepatomegaly.
Lung cancer causes chronic central cyanosis accompanied by fever, weakness, weight loss, anorexia, dyspnea, chest pain, hemoptysis, and wheezing. Atelectasis causes mediastinal shift, decreased diaphragmatic excursion, asymmetrical chest expansion, a dull percussion note, and diminished breath sounds.
Peripheral arterial occlusion produces acute cyanosis of one arm or leg or, occasionally, of both legs. The cyanosis is accompanied by sharp or aching pain that worsens when the patient moves. The affected extremity also exhibits paresthesia, weakness, and pale, cool skin. Examination reveals decreased or absent pulse and increased capillary refill time.
With pneumonia, acute central cyanosis is usually preceded by fever, shaking chills, cough with purulent sputum, crackles, rhonchi, and pleuritic chest pain that’s exacerbated by deep inspiration. Associated signs and symptoms include tachycardia, dyspnea, tachypnea, diminished breath sounds, diaphoresis, myalgia, fatigue, headache, and anorexia.
A cardinal sign of pneumothorax, acute central cyanosis is accompanied by sharp chest pain that’s exacerbated by movement, deep breathing, and coughing. The patient exhibits asymmetrical chest wall expansion, shortness of breath, and pallor. He may also experience jugular vein distention, anxiety, absence of breath sounds over the affected lobe, and rapid, shallow respirations. His pulse may be weak and rapid.
Polycythemia vera.
A ruddy complexion that can appear cyanotic is characteristic in polycythemia vera — a chronic myeloproliferative disorder. Other findings include hepatosplenomegaly, headache, dizziness, fatigue, aquagenic pruritus, blurred vision, chest pain, intermittent claudication, and coagulation defects.
Pulmonary edema.
With pulmonary edema, acute central cyanosis occurs with dyspnea, orthopnea, tachycardia, tachypnea, dependent crackles, ventricular gallop, hypotension, confusion, and frothy, blood-tinged sputum. The patient may exhibit cold, clammy skin and a weak, thready pulse.
Pulmonary embolism.
Acute central cyanosis occurs when a large embolus causes significant obstruction of the pulmonary circulation. Syncope and jugular vein distention may also occur. Other common signs and symptoms include dyspnea, chest pain, tachycardia, paradoxical pulse, dry or productive cough with blood-tinged sputum, low-grade fever, restlessness, and diaphoresis.
Raynaud’s disease.
With Raynaud’s disease, exposure to cold or stress causes the fingers or hands to blanch and turn cold, become cyanotic, and finally redden with return of normal temperature. Numbness and tingling may also occur. Raynaud’s phenomenon describes the same presentation when associated with other disorders, such as rheumatoid arthritis, scleroderma, or lupus erythematosus.
With shock, acute peripheral cyanosis develops in the hands and feet, which may also be cold, clammy, and pale. Other characteristic signs and symptoms include lethargy, confusion, increased capillary refill time, and a rapid, weak pulse. Tachypnea, hyperpnea, and hypotension may also be present.
Sleep apnea.
When chronic and severe, sleep apnea causes pulmonary hypertension and cor pulmonale (right-sided heart failure), which can produce chronic cyanosis.
Nursing considerations
Provide supplemental oxygen to relieve shortness of breath, improve oxygenation, and decrease cyanosis. However, deliver small doses (2 L/minute) in the patient with COPD, who may retain carbon dioxide. Use a low-flow oxygen rate for mild COPD exacerbations. However, for acute situations, a high-flow oxygen rate may be needed initially. Simply remember to be attentive to the patient’s respiratory drive and adjust the amount of oxygen accordingly. Position the patient comfortably to ease breathing. Administer a diuretic, bronchodilator, antibiotic, or cardiac drug as needed. Make sure that the patient gets sufficient rest between activities to prevent dyspnea.
Prepare the patient for such tests as arterial blood gas analysis and complete blood count to determine the cause of cyanosis.
Patient teaching
Teach patients with chronic cardiopulmonary diseases, such as heart failure, asthma, or COPD, to recognize cyanosis as a sign of severe disease requiring immediate medical attention.
Book Source Details
- Book Title: Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series
- Author(s): Springhouse
- Year of Publication: 2007
- Copyright Details: Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series, Copyright © 2007 Lippincott Williams & Wilkins.
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Copyright Details: Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series, Copyright © 2008 Williams & Wilkins.
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