Air embolism is the migration of a bolus of gas from the systemic circulation into the microvasculature. Obstruction occurs when the gas reaches the capillary system. Besides impairing blood flow, an air embolus causes a physiologic response as fibrin, platelets, and red blood cells congregate at the site of occlusion. This further restricts blood flow and contributes to an inflammatory vasospasm of the affected vessel.
Arterial air emboli may lodge in the small vessels that supply major organs or the peripheral circulation. Venous air emboli commonly occlude pulmonary blood flow; they may also obstruct arterial circulation if the patient has an intracardiac defect or a microvascular shunt between the arterioles and venules of the lungs.
A bolus of air may enter the bloodstream during positive-pressure ventilation if the patient has a lung tear, or when air enters an artery or vein during insertion, maintenance, or removal of the arterial or venous line. Air emboli have also been associated with oralvaginal sex, laser surgery, and pneumoperitoneum. They may also occur as a complication of needle biopsy or pregnancy. Air emboli also result from rapid decompression after underwater diving.
Venous air emboli may occur as a complication of surgery or blunt or penetrating trauma to the head, neck, chest, heart, or abdomen.
Signs and symptoms
The first sign of a venous air embolism may be cardiopulmonary collapse, especially in the presence of a rapid infusion of a large volume of air.
If the embolus moves into the arterial circulation, central nervous system and cardiac symptoms may develop. The patient may have dyspnea, vertigo, anxiety, or a sense of impending doom. He may also experience a “gasp” reflex (cough, short exhalation, and prolonged inhalation).
Other signs include tachycardia, tachypnea, hypoxemia, and elevated central venous and pulmonary artery pressures. Electrocardiogram results show ST-segment changes that reflect ischemia. A transient churning heart murmur has been noted. Hypotension and decreased peripheral vascular resistance indicate progressive shock. Crepitus occasionally is palpable, and wheezes and crackles may be auscultated when pulmonary edema is present.
The goal of treatment is to promote reabsorption of trapped air and mitigate life-threatening signs and symptoms. In the event of cardiac arrest, cardiopulmonary resuscitation (CPR) is initiated immediately. External cardiac massage improves circulation and may help break up large right ventricular bubbles, increasing blood flow to the pulmonary vasculature.
An air embolus may be removed through a central venous catheter or by needle aspiration. The size of the bubble may be reduced by administering 100% oxygen, which reduces the amount of nitrogen in the bubble, or by administering hyperbaric oxygen; the latter approach may also improve the patient’s signs and symptoms by oxygenating ischemic tissue.
♦ Preventing air embolism is the key to nursing care. Make sure that all air is purged from catheters and I.V. lines before connecting them.
♦ Keep closed systems as airtight as possible; tape all tubing connections, or use luer-lock devices for all connections.
♦ Place the patient in Trendelenburg’s position when inserting all central venous line catheters. Have the patient perform Valsalva’s maneuver during catheter insertion and tubing changes.
♦ Position the patient on his left side in Trendelenburg’s position so that air can enter the right atrium and be dispersed by the pulmonary artery.
♦ Initiate CPR immediately if cardiac collapse occurs.
In atelectasis, alveolar clusters (lobules) or lung segments don’t expand completely during respiration, causing all or part of the affected lung to collapse. This condition can be acute or chronic. Because the collapsed lung tissue is effectively isolated from gas exchange, unoxygenated blood is shunted and passes unchanged through these tissues, producing hypoxia.
Atelectasis can result from bronchial occlusion by mucus plugs—a problem for patients with chronic obstructive pulmonary disease, bronchiectasis, or cystic fibrosis. Atelectasis may also result from occlusion caused by foreign bodies, bronchogenic cancer, or inflammatory lung disease.
Other causes include idiopathic respiratory distress syndrome of the neonate, oxygen toxicity, and pulmonary edema.
External compression, which inhibits full lung expansion, or any condition that makes deep breathing painful may also cause atelectasis. Compression or pain may result from surgical incisions in the upper abdomen, rib fractures, pleuritic chest pain, tight chest dressings, or obesity (which elevates the diaphragm and reduces tidal volume).
Lung collapse or reduced expansion may accompany prolonged immobility or mechanical ventilation. Central nervous system depression eliminates periodic sighing and predisposes the patient to progressive atelectasis.
Signs and symptoms
Clinical effects vary with the causes of lung collapse, the degree of hypoxia, and the underlying disease. If atelectasis affects a small area of the lung, symptoms may be minimal and transient; however, if atelectasis affects a large area, symptoms may be severe and may include dyspnea, tachypnea, tachycardia, anxiety, and pleuritic chest pain.
Inspection may show decreased movement of the chest wall, cyanosis, diaphoresis, and substernal or intercostal retractions. Palpation may show decreased fremitus and a mediastinal shift to the affected side. Percussion may show dullness or flatness over the lung fields. Auscultation may show crackles during the last part of inspiration and decreased (or absent) breath sounds with major lung involvement; auscultation may also disclose tachycardia.
A chest X-ray is the primary diagnostic tool. Other diagnostic tests include bronchoscopy to rule out an obstructing neoplasm or a foreign body, arterial blood gas (ABG) analysis to detect respiratory acidosis and hypoxemia resulting from atelectasis, and pulse oximetry, which may show deteriorating arterial oxygen saturation levels.
Incentive spirometry, chest percussion, postural drainage, mucolytics, and frequent coughing and deep-breathing exercises may improve oxygenation. If these measures are unsuccessful, bronchoscopy may help to remove secretions. Humidity and a bronchodilator
can improve mucociliary clearance and dilate the airways.
To minimize the risk of atelectasis after thoracic and abdominal surgery, the patient may require an analgesic to facilitate deep breathing. If the patient has atelectasis as a result of an obstructing neoplasm, he may need surgery or radiation therapy.
♦ Offer the patient reassurance and emotional support because he may be frightened by his limited ability to breathe.
♦ Encourage a patient who is recovering from surgery to perform coughing and deep-breathing exercises and incentive spirometry every 1 to 2 hours while splinting the incision. Encourage these procedures in any patient who is at increased risk for atelectasis.
♦ Assess the patient’s breath sounds and respiratory status frequently. Report changes immediately; monitor pulse oximetry readings and ABG values for evidence of hypoxia.
♦ Gently reposition the patient often, and help him walk as soon as possible. Administer adequate analgesics to control his pain.
♦ If the patient is receiving mechanical ventilation, maintain the tidal volume at 10 to 15 cc/kg of body weight to ensure adequate lung expansion. Use the sigh mechanism on the ventilator, if appropriate, to increase the tidal volume intermittently at the rate of 10 to 15 sighs per hour.
♦ Humidify inspired air, and encourage adequate fluid intake to mobilize secretions. Use postural drainage and chest percussion to remove secretions. Suction as needed.
♦ Administer sedatives cautiously. They depress respirations and the cough reflex and suppress sighs.
Bone marrow suppression
Bone marrow suppression is characterized by reduced numbers of hematopoietic (blood-forming) stem cells in the bone marrow. Impaired hematopoiesis leads to reduced numbers of peripheral blood leukocytes and neutrophils (neutropenia), thrombocytes (thrombocytopenia), and erythrocytes (anemia).
Many chemotherapeutic agents injure the rapidly proliferating stem cells. Other drugs, such as sulfa compounds, anticonvulsants, and immunosuppressants, also may suppress bone marrow.
Radiation to large marrow-bearing areas—such as the pelvis, ribs, spine, and sternum—may produce significant, permanent bone marrow damage. Bone marrow suppression and depressed peripheral blood cell counts occur in patients with tumor replacement of the bone marrow (leukemia, myeloma, or metastatic deposits from solid tumors). Additional causes of bone marrow suppression include autoimmune disorders, certain congenital disorders, and exposure to pesticides, benzene-containing solvents, and other toxins.
Signs and symptoms
Clinical effects of bone marrow suppression are related to its severity. A patient with neutropenia is at risk for infection from bacteria, viruses, or fungi. He may have fever, chills, malaise, or other localized signs of infection.
Thrombocytopenia is associated with bleeding (especially from the gums and nose), bruising, petechiae, ecchymoses, hematuria and, possibly, hematochezia. Spontaneous bleeding is likely to occur if the platelet count drops below 20,000/mm3.
Signs and symptoms of anemia include fatigue, weakness, pallor, tachycardia,
palpitations, dizziness, exertional dyspnea, and headache.
Improved antimicrobial therapy has dramatically reduced the rates of morbidity and mortality in patients with neutropenia. Chemotherapy-induced neutropenia can be reduced by the use of myeloid growth factors (granulocyte colony-stimulating factor [filgrastim] or granulocyte-macrophage colonystimulating factor [sargramostim]).
In patients with drug-induced thrombocytopenia, removal of the causative agents or proper treatment of the underlying cause (when possible) is essential. A corticosteroid, lithium carbonate, or folate may be used to increase platelet production. Platelet transfusions may be used to stop episodic abnormal bleeding caused by a low platelet count; however, if platelet destruction is caused by an immune disorder, platelet infusions may have only a minimal effect and may be reserved for life-threatening bleeding.
Recombinant erythropoietin may help improve anemia caused by chronic disease or renal dysfunction. Packed red blood cells and platelets are administered to support the patient until bone marrow function recovers.
See Nursing interventions in bone marrow suppression.
Brain herniation is caused by distortion and displacement of brain tissue through a natural opening in the intracranial cavity.
Five types of brain herniation syndrome occur: central, uncal, tonsillar, cingulate, and extracranial. Central herniation—also known as transtentorial herniation—is an upward or downward displacement of the temporal lobe and diencephalon through the tentorium. In uncal herniation, the inner part of the temporal lobe passes the tentorium and presses on the brain stem. In tonsillar herniation, the tonsils of the cerebellum pass down through the foramen magnum and press on the brain stem and spinal cord, possibly causing respiratory and cardiac dysfunction. Cingulate, or subfalcine, herniation involves displacement of the frontal lobe of the brain under the falx cerebri. Finally, in extracranial herniation, the brain is displaced through a cranial defect, such as a fracture or a craniotomy.
Brain herniation is caused by spaceoccupying lesions, cerebral edema as a result of trauma or stroke, or hydrocephalus. It can also be caused by excessive drainage of cerebrospinal fluid (CSF) from a ventricular catheter or lumbar puncture.
Signs and symptoms
Signs and symptoms vary with the type of herniation. General early signs include decreasing level of consciousness, pupillary abnormalities, impaired motor function, and impaired brain stem reflexes. Signs of central herniation include small, reactive pupils (early phase); roving eye movements with loss of upward gaze; intermittent agitation and drowsiness progressing to stupor; contralateral hemiparesis; and Cheyne-Stokes respirations. Signs of transtentorial herniation include ipsilateral pupil dilation, paralysis of eye movements, restlessness progressing to loss of consciousness, contralateral hemiparesis, decorticate or decerebrate posturing, and bilateral Babinski’s sign. Late in the syndrome, altered vital signs become evident, such as widening pulse pressure and bradycardia.
If herniation is caused by a spaceoccupying lesion, such as a hematoma or tumor, surgical removal of the lesion will relieve the pressure and allow adjacent structures to resume their normal shape. If herniation is related to increased intracranial pressure (ICP) as a result of cerebral edema, treatment involves reducing the edema with an osmotic diuretic or a corticosteroid, CSF drainage, hyperventilation and, in extreme cases, barbiturate therapy. Maintaining temperature control and a normal fluid balance is also important. In some situations, such as cerebral edema caused by traumatic injury, the patient may have an ICP monitor in place to help guide treatment.
♦ Perform a neurologic assessment at least hourly.
♦ Institute precautionary measures to decrease ICP, including elevating the head of the bed at 15 to 30 degrees to promote venous drainage. Place the patient in a neutral position, avoiding extreme hip and neck flexion.
♦ Institute seizure precautions, and assess the patient frequently for signs of seizures.
♦ Monitor the patient’s vital signs frequently to ensure adequate cerebral perfusion.
♦ If the patient underwent a craniotomy for a hematoma or tumor, provide postoperative craniotomy care.
♦ Observe the patient carefully for other postoperative complications, such as infection, thrombophlebitis, or diabetes insipidus.
In cardiac tamponade, a rapid, unchecked increase in intrapericardial pressure impairs diastolic filling of the heart. The increased pressure usually results from the accumulation of blood or fluid in the pericardial sac. If fluid accumulates rapidly, as little as 250 ml can create an emergency situation. Gradual accumulation of fluid, as in pericardial effusion associated with cancer, may not produce immediate signs and symptoms because the fibrous wall of the pericardial sac can stretch to accommodate as much as 1 to 2 L of fluid.
Cardiac tamponade may be idiopathic (Dressler’s syndrome), or it may result from effusion (in lung cancer, bacterial infection, tuberculosis, lupus and, rarely, acute rheumatic fever), hemorrhage as a result of trauma, hemorrhage from nontraumatic causes (with pericarditis), acute myocardial infarction, chronic renal failure during dialysis, drug reaction, or a connective tissue disorder.
Signs and symptoms
Cardiac tamponade classically produces increased venous pressure, with jugular vein distention, reduced arterial blood pressure, muffled heart sounds on auscultation, and paradoxical pulse (an abnormal inspiratory drop in systemic blood pressure greater than 15 mm Hg).
Cardiac tamponade may also cause dyspnea, diaphoresis, pallor or cyanosis, anxiety, tachycardia, narrowed pulse pressure, restlessness, and hepatomegaly, but the lung fields will be clear. The patient typically sits upright and leans forward.
Chest X-rays show a slightly widened mediastinum and an enlarged cardiac silhouette. Electrocardiography is performed to rule out other cardiac disorders. Pulmonary artery pressure monitoring detects increases in right atrial pressure, right ventricular diastolic pressure, and central venous pressure (CVP). Echocardiography records pericardial effusion with signs of right ventricular and atrial compression.
The goal of treatment is to relieve intrapericardial pressure and cardiac compression by removing accumulated blood or fluid. Pericardiocentesis (needle aspiration of the pericardial cavity) or surgical creation of an opening dramatically improves systemic arterial pressure and cardiac output with the aspiration of as little as 25 ml of fluid.
In a patient with hypotension, trial volume loading with normal saline solution I.V. with albumin—and perhaps an inotropic drug such as dopamine— is necessary to maintain cardiac output. Depending on the cause of tamponade, additional treatment may be needed.
♦ Infuse I.V. solutions and inotropic drugs (such as dopamine), as ordered, to maintain the patient’s blood pressure.
♦ Administer oxygen therapy as needed.
♦ Prepare the patient for pericardiocentesis, thoracotomy, or central venous line insertion, as indicated.
♦ Check for signs of increasing tamponade, increasing dyspnea, and arrhythmias.
♦ Watch for a decrease in CVP and a concomitant rise in blood pressure
after treatment; these indicate relief of cardiac compression.
♦ Monitor the patient’s respiratory status for signs of respiratory distress, such as severe tachypnea or changes in the level of consciousness.
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