UNDERSTANDING TENSION PNEUMOTHORAX

In tension pneumothorax, air accumulates intrapleurally and cannot escape. As intrapleural pressure rises, the ipsilateral lung is affected and also collapses.

Signs and symptoms

The following signs and symptoms may occur:

sudden, sharp pleuritic pain exacerbated by chest movement, breathing, and coughing asymmetrical chest wall movement due to collapse of the lung

shortness of breath due to hypoxia cyanosis due to hypoxia

respiratory distress

decreased vocal fremitus related to collapse of the lung

absent breath sounds on the affected side due to collapse of the lung chest rigidity on the affected side due to decreased expansion

tachycardia due to hypoxia

crackling beneath the skin on palpation (subcutaneous emphysema), which is due to air leaking into the tissues.

Tension pneumothorax produces the most severe respiratory symptoms, including:

decreased cardiac output

hypotension due to decreased cardiac output compensatory tachycardia

tachypnea due to hypoxia

lung collapse due to air or blood in the intrapleural space mediastinal shift due to increasing tension

tracheal deviation to the opposite side

distended neck veins due to intrapleural pressure, mediastinal shift, and increased cardiovascular pressure pallor related to decreased cardiac output

anxiety related to hypoxia

weak and rapid pulse due to decreased cardiac output.

Complications

Possible complications include:

decreased cardiac output hypoxemia

cardiac arrest.

Diagnosis

The following tests help diagnose pneumothorax:

Chest X-rays confirm the diagnosis by revealing air in the pleural space and, possibly, a mediastinal shift.

Arterial blood gas analysis may reveal hypoxemia, possibly with respiratory acidosis and hypercapnia. Pa O₂ levels may decrease at first, but typically return to normal within 24 hours.

Treatment

Treatment depends on the type of pneumothorax.

Spontaneous pneumothorax with less than 30% of lung collapse, no signs of increased pleural pressure, and no dyspnea or indications of physiologic compromise, may be corrected with:

bed rest to conserve energy and reduce oxygenation demands

monitoring of blood pressure and pulse for early detection of physiologic compromise monitoring of respiratory rate to detect early signs of respiratory compromise

oxygen administration to enhance oxygenation and improve hypoxia

aspiration of air with a large-bore needle attached to a syringe to restore negative pressure within the pleural space.

Correction of pneumothorax with more than 30% of lung collapse may include:

thoracostomy tube placed in the second or third intercostal space in the midclavicular line to try to re-expand the lung by restoring negative intrapleural pressure

connection of the thoracostomy tube to underwater seal or to low-pressure suction to re-expand the lung

if recurrent spontaneous pneumothorax, thoracotomy and pleurectomy may be performed, which causes the lung to adhere to the parietal pleura.

Open (traumatic) pneumothorax may be corrected with:

chest tube drainage to re-expand the lung surgical repair of the lung.

Correction of tension pneumothorax typically involves:

immediate treatment with large-bore needle insertion into the pleural space through the second intercostal space to re-expand the lung

insertion of a thoracostomy tube if large amounts of air escape through the needle after insertion analgesics to promote comfort and encourage deep breathing and coughing.

Pulmonary edema

Pulmonary edema is an accumulation of fluid in the extravascular spaces of the lungs. It is a common complication of cardiac disorders and may occur as a chronic condition or may develop quickly and rapidly become fatal.

Causes

Pulmonary edema is caused by left-sided heart failure due to:

arteriosclerosis cardiomyopathy hypertension

valvular heart disease.

Factors that predispose the patient to pulmonary edema include:

barbiturate or opiate poisoning cardiac failure

infusion of excessive volume of intravenous fluids or overly rapid infusion

impaired pulmonary lymphatic drainage (from Hodgkin's disease or obliterative lymphangitis after radiation) inhalation of irritating gases

mitral stenosis and left atrial myxoma (which impairs left atrial emptying) pneumonia

pulmonary venoocclusive disease.

Pathophysiology

Normally, pulmonary capillary hydrostatic pressure, capillary oncotic pressure, capillary permeability, and lymphatic drainage are in balance. When this balance changes, or the lymphatic drainage system is obstructed, fluid infiltrates into the lung and pulmonary edema results. If pulmonary capillary hydrostatic pressure increases, the compromised left ventricle requires increased filling pressures to maintain adequate cardiac output. These pressures are transmitted to the left atrium, pulmonary veins, and pulmonary capillary bed, forcing fluids and solutes from the intravascular compartment into the interstitium of the lungs. As the interstitium overloads with fluid, fluid floods the peripheral alveoli and impairs gas

exchange.

If colloid osmotic pressure decreases, the hydrostatic force that regulates intravascular fluids (the natural pulling force) is lost because there is no opposition. Fluid flows freely into the interstitium and alveoli, impairing gas exchange and

leading to pulmonary edema. (See Understanding pulmonary edema.)

A blockage of the lymph vessels can result from compression by edema or tumor fibrotic tissue, and by increased systemic venous pressure. Hydrostatic pressure in the large pulmonary veins rises, the pulmonary lymphatic system cannot drain correctly into the pulmonary veins, and excess fluid moves into the interstitial space. Pulmonary edema then results from the accumulation of fluid.

Capillary injury, such as occurs in adult respiratory distress syndrome or with inhalation of toxic gases, increases capillary permeability. The injury causes plasma proteins and water to leak out of the capillary and move into the interstitium, increasing the interstitial oncotic pressure, which is normally low. As interstitial oncotic pressure begins to equal capillary oncotic pressure, the water begins to move out of the capillary and into the lungs, resulting in pulmonary edema.

Signs and symptoms

Early signs and symptoms may include:

dyspnea on exertion due to hypoxia

paroxysmal nocturnal dyspnea due to decreased expansion of the lungs orthopnea due to decreased ability of the diaphragm to expand

cough due to stimulation of cough reflex by excessive fluid mild tachypnea due to hypoxia

increased blood pressure due to increased pulmonary pressures and decreased oxygenation dependent crackles as air moves through fluid in the lungs

neck vein distention due to decreased cardiac output and increased pulmonary vascular resistance tachycardia due to hypoxia.

Later stages of pulmonary edema may include the following signs and symptoms:

labored, rapid respiration due to hypoxia

more diffuse crackles as air moves through fluid in the lungs cough, producing frothy, bloody sputum

increased tachycardia due to hypoxemia arrhythmias due to hypoxic myocardium

cold, clammy skin due to peripheral vasoconstriction diaphoresis due to decreased cardiac output and shock cyanosis due to hypoxia

decreased blood pressure due to decreased cardiac output and shock thready pulse due to decreased cardiac output and shock.

Complications

Possible complications include:

respiratory failure respiratory acidosis cardiac arrest.

Diagnosis

The following tests help diagnose pulmonary edema:

Arterial blood gas analysis usually reveals hypoxia with variable Pa CO₂, depending on the patient's degree of fatigue. Respiratory acidosis may occur.

Chest X-rays show diffuse haziness of the lung fields and, usually, cardiomegaly and pleural effusion.

Pulse oximetry may reveal decreasing SaO₂ levels.

Pulmonary artery catheterization identifies left-sided heart failure and helps rule out adult respiratory distress syndrome.

Electrocardiography may show previous or current myocardial infarction.