Pneumothorax

Pneumothorax is an accumulation of air in the pleural cavity that leads to partial or complete lung collapse. When the air between the visceral and parietal pleurae collects and accumulates, increasing tension in the pleural cavity can cause the lung to progressively collapse. Air is trapped in the intrapleural space and determines the degree of lung collapse. Venous return to the heart may be impeded to cause a life-threatening condition called tension pneumothorax. The most common types of pneumothorax are open, closed, and tension. Causes Common causes of open pneumothorax include: penetrating chest injury (gunshot or stab wound) insertion of a central venous catheter chest surgery transbronchial biopsy thoracentesis or closed pleural biopsy. Causes of closed pneumothorax include: blunt chest trauma air leakage from ruptured blebs rupture resulting from barotrauma caused by high intrathoracic pressures during mechanical ventilation tubercular or cancerous lesions that erode into the pleural space interstitial lung disease, such as eosinophilic granuloma. Tension pneumothorax may be caused by: penetrating chest wound treated with an air-tight dressing fractured ribs mechanical ventilation high-level positive end-expiratory pressure that causes alveolar blebs to rupture chest tube occlusion or malfunction. Pathophysiology A rupture in the visceral or parietal pleura and chest wall causes air to accumulate and separate the visceral and parietal pleurae. Negative pressure is destroyed and the elastic recoil forces are affected. The lung recoils by collapsing toward the hilus. Open pneumothorax (also called sucking chest wound or communicating pneumothorax) results when atmospheric air (positive pressure) flows directly into the pleural cavity (negative pressure). As the air pressure in the pleural cavity becomes positive, the lung collapses on the affected side, resulting in decreased total lung capacity, vital capacity, and lung compliance. / imbalances lead to hypoxia. Closed pneumothorax occurs when air enters the pleural space from within the lung, causing increased pleural pressure, which prevents lung expansion during normal inspiration. Spontaneous pneumothorax is another type of closed pneumothorax.

AGE ALERT Spontaneous pneumothorax is common in older patients with chronic pulmonary disease, but it may also occur in healthy, tall, young adults. Both types of closed pneumothorax can result in a collapsed lung with hypoxia and decreased total lung capacity, vital capacity, and lung compliance. The range of lung collapse is between 5% and 95%. Tension pneumothorax results when air in the pleural space is under higher pressure than air in the adjacent lung. The air enters the pleural space from the site of pleural rupture, which acts as a one-way valve. Air is allowed to enter into the pleural space on inspiration but cannot escape as the rupture site closes on expiration. More air enters on inspiration and air pressure begins to exceed barometric pressure. Increasing air pressure pushes against the recoiled lung, causing compression atelectasis. Air also presses against the mediastinum, compressing and displacing the heart and great vessels. The air cannot escape, and the accumulating pressure causes the lung to collapse. As air continues to accumulate and intrapleural pressures rise, the mediastinum shifts away from the affected side and decreases venous return. This forces the heart, trachea, esophagus, and great vessels to the unaffected side, compressing the heart and the contralateral lung. Without immediate treatment, this emergency can rapidly become fatal. (See Understanding tension pneumothorax.)

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.

Treatment Correcting this disorder typically involves: high concentrations of oxygen administered by nasal cannula to enhance gas exchange and improve oxygenation assisted ventilation to improve oxygen delivery to the tissues and promote acid-base balance diuretics, such as furosemide, ethacrynic acid, and bumetanide, to increase urination, which helps mobilize extravascular fluid positive inotropic agents, such as digoxin and amrinone, to enhance contractility in myocardial dysfunction

pressor agents to enhance contractility and promote vasoconstriction in peripheral vessels antiarrhythmics for arrhythmias related to decreased cardiac output arterial vasodilators such as nitroprusside to decrease peripheral vascular resistance, preload, and afterload morphine to reduce anxiety and dyspnea, and to dilate the systemic venous bed, promoting blood flow from pulmonary circulation to the periphery.

Pulmonary hypertension
Pulmonary hypertension is indicated by a resting systolic pulmonary artery pressure (PAP) above 30 mm Hg and a mean PAP above 18 mm Hg. Primary or idiopathic pulmonary hypertension is characterized by increased PAP and increased pulmonary vascular resistance. This form is most common in women ages 20 to 40 and is usually fatal within 3 to 4 years. AGE ALERT Mortality is highest in pregnant women. Secondary pulmonary hypertension results from existing cardiac or pulmonary disease, or both. The prognosis in secondary pulmonary hypertension depends on the severity of the underlying disorder. The patient may have no signs or symptoms of the disorder until lung damage becomes severe. In fact, it may not be diagnosed until an autopsy is performed. Causes Causes of primary pulmonary hypertension are unknown, but may include: hereditary factors altered immune mechanisms. Secondary pulmonary hypertension results from hypoxemia as the result of the following. Conditions causing alveolar hypoventilation: chronic obstructive pulmonary disease sarcoidosis diffuse interstitial pneumonia malignant metastases obesity kyphoscoliosis. Conditions causing vascular obstruction: pulmonary embolism vasculitis left atrial myxoma idiopathic venoocclusive disease fibrosing mediastinitis mediastinal neoplasm. Conditions causing primary cardiac disease: patent ductus arteriosus atrial septal defect

ventricular septal defect. Conditions causing acquired cardiac disease: rheumatic valvular disease mitral stenosis. Pathophysiology In primary pulmonary hypertension, the smooth muscle in the pulmonary artery wall hypertrophies for no reason, narrowing the small pulmonary artery (arterioles) or obliterating it completely. Fibrous lesions also form around the vessels, impairing distensibility and increasing vascular resistance. Pressures in the left ventricle, which receives blood from the lungs, remain normal. However, the increased pressures generated in the lungs are transmitted to the right ventricle, which supplies the pulmonary artery. Eventually, the right ventricle fails (cor pulmonale). Although oxygenation is not severely affected initially, hypoxia and cyanosis eventually occur. Death results from cor pulmonale. Alveolar hypoventilation can result from diseases caused by alveolar destruction or from disorders that prevent the chest wall from expanding sufficiently to allow air into the alveoli. The resulting decreased ventilation increases pulmonary vascular resistance. Hypoxemia resulting from this / mismatch also causes vasoconstriction, further increasing vascular resistance and resulting in pulmonary hypertension. Coronary artery disease or mitral valvular disease causing increased left ventricular filling pressures may cause secondary pulmonary hypertension. Ventricular septal defect and patent ductus arteriosus cause secondary pulmonary hypertension by increasing blood flow through the pulmonary circulation via left-toright shunting. Pulmonary emboli and chronic destruction of alveolar walls, as in emphysema, cause secondary pulmonary hypertension by obliterating or obstructing the pulmonary vascular bed. Secondary pulmonary hypertension can also occur by vasoconstriction of the vascular bed, such as through hypoxemia, acidosis, or both. Conditions resulting in vascular obstruction can also cause pulmonary hypertension because blood is not allowed to flow appropriately through the vessels. Secondary pulmonary hypertension can be reversed if the disorder is resolved. If hypertension persists, hypertrophy occurs in the medial smooth muscle layer of the arterioles. The larger arteries stiffen and hypertension progresses. Pulmonary pressures begin to equal systemic blood pressure, causing right ventricular hypertrophy and eventually cor pulmonale. Primary cardiac diseases may be congenital or acquired. Congenital defects cause a left-to-right shunt, re-routing blood through the lungs twice and causing pulmonary hypertension. Acquired cardiac diseases, such as rheumatic valvular

disease and mitral stenosis, result in left ventricular failure that diminishes the flow of oxygenated blood from the lungs. This increases pulmonary vascular resistance and right ventricular pressure. Signs and symptoms The following signs and symptoms may occur: increasing dyspnea on exertion from left ventricular failure fatigue and weakness from diminished oxygenation to the tissues syncope due to diminished oxygenation to brain cells difficulty breathing due to left ventricular failure shortness of breath due to left ventricular failure pain with breathing due to lactic acidosis buildup in the tissues ascites due to right ventricular failure neck vein distention due to right ventricular failure restlessness and agitation due to hypoxia decreased level of consciousness, confusion, and memory loss due to hypoxia decreased diaphragmatic excursion and respiration due to hypoventilation possible displacement of point of maximal impulse beyond the midclavicular line due to fluid accumulation peripheral edema due to right ventricular failure easily palpable right ventricular lift due to altered cardiac output and pulmonary hypertension reduced carotid pulse palpable and tender liver due to pulmonary hypertension tachycardia due to hypoxia systolic ejection murmur due to pulmonary hypertension and altered cardiac output split S2, S3, and S4 sounds due to pulmonary hypertension and altered cardiac output decreased breath sounds due to fluid accumulation in the lungs loud, tubular breath sounds due to fluid accumulation in the lungs. Complications Possible complications of pulmonary hypertension include: cor pulmonale cardiac failure cardiac arrest. Diagnosis The following tests help diagnose pulmonary hypertension: Arterial blood gas analysis reveals hypoxemia. Electrocardiography in right ventricular hypertrophy shows right axis deviation and tall or peaked P waves in inferior leads. Cardiac catheterization reveals increased PAP, with systolic pressure above 30 mm Hg. It may also show an increased pulmonary capillary wedge pressure (PCWP) if the underlying cause is left atrial myxoma, mitral stenosis, or left ventricular failure; otherwise, PCWP is normal. Pulmonary angiography detects filling defects in pulmonary vasculature, such as those that develop with pulmonary emboli. Pulmonary function studies may show decreased flow rates and increased residual volume in underlying obstructive

disease; in underlying restrictive disease, they may show reduced total lung capacity. Radionuclide imaging detects abnormalities in right and left ventricular functioning. Open lung biopsy may determine the type of disorder. Echocardiography allows the assessment of ventricular wall motion and possible valvular dysfunction. It can also demonstrate right ventricular enlargement, abnormal septal configuration consistent with right ventricular pressure overload, and reduction in left ventricular cavity size. Perfusion lung scanning may produce normal or abnormal results, with multiple patchy and diffuse filling defects that don't suggest pulmonary embolism. Treatment Managing this disorder typically involves: oxygen therapy to correct hypoxemia and resulting increased pulmonary vascular resistance fluid restriction in right ventricular failure to decrease workload of the heart digoxin to increase cardiac output diuretics to decrease intravascular volume and extravascular fluid accumulation vasodilators to reduce myocardial workload and oxygen consumption calcium channel blockers to reduce myocardial workload and oxygen consumption bronchodilators to relax smooth muscles and increase airway patency beta-adrenergic blockers to improve oxygenation treatment of the underlying cause to correct pulmonary edema heart-lung transplant in severe cases.

Cor pulmonale Cor pulmonale (also called right ventricular failure) is a condition in which hypertrophy and dilation of the right ventricle develop secondary to disease affecting the structure or function of the lungs or their vasculature. It can occur at the end stage of various chronic disorders of the lungs, pulmonary vessels, chest wall, and respiratory control center. Cor pulmonale doesn't occur with disorders stemming from congenital heart disease or with those affecting the left side of the heart. CULTURAL DIVERSITY Cor pulmonale is more prevalent in countries where the incidence of obstructive lung disease is high, such as in the United Kingdom. About 85% of patients with cor pulmonale also have chronic obstructive pulmonary disease (COPD), and about 25% of patients with bronchial COPD eventually develop cor pulmonale. The disorder is most common in smokers and in middle-aged and elderly males; however, its incidence in females is rising. Because cor pulmonale occurs late in the course of the individual's underlying condition and with other irreversible diseases, the prognosis is poor.

AGE ALERT In children, cor pulmonale may be a complication of cystic fibrosis, hemosiderosis, upper airway obstruction, scleroderma, extensive bronchiectasis, neuromuscular diseases that affect respiratory muscles, or abnormalities of the respiratory control area. Causes Common causes of cor pulmonale include: disorders that affect the pulmonary parenchyma COPD bronchial asthma primary pulmonary hypertension vasculitis pulmonary emboli external vascular obstruction resulting from a tumor or aneurysm kyphoscoliosis pectus excavatum (funnel chest) muscular dystrophy poliomyelitis obesity high altitude. Pathophysiology In cor pulmonale, pulmonary hypertension increases the heart's workload. To compensate, the right ventricle hypertrophies to force blood through the lungs. As long as the heart can compensate for the increased pulmonary vascular resistance, signs and symptoms reflect only the underlying disorder. Severity of right ventricular enlargement in cor pulmonale is due to increased afterload. An occluded vessel impairs the heart's ability to generate enough pressure. Pulmonary hypertension results from the increased blood flow needed to oxygenate the tissues. In response to hypoxia, the bone marrow produces more red blood cells, causing polycythemia. The blood's viscosity increases, which further aggravates pulmonary hypertension. This increases the right ventricle's workload, causing heart failure. (See Cor pulmonale: An overview.) In chronic obstructive disease, increased airway obstruction makes airflow worse. The resulting hypoxia and hypercarbia can have vasodilatory effects on systemic arterioles. However, hypoxia increases pulmonary vasoconstriction. The liver becomes palpable and tender because it is engorged and displaced downward by the low diaphragm. Hepatojugular reflux may occur. Compensatory mechanisms begin to fail and larger amounts of blood remain in the right ventricle at the end of diastole, causing ventricular dilation. Increasing intrathoracic pressures impede venous return and raise jugular venous pressure. Peripheral edema can occur and right ventricular hypertrophy increases progressively. The main pulmonary arteries enlarge, pulmonary hypertension increases, and heart failure occurs.

Signs and symptoms Patients in early stages of cor pulmonale may present with: chronic productive cough to clear secretions from the lungs exertional dyspnea due to hypoxia wheezing respirations as airways narrow fatigue and weakness due to hypoxemia. Patients with progressive cor pulmonale may present with: dyspnea at rest due to hypoxemia tachypnea due to response to decreased oxygenation to the tissues orthopnea due to pulmonary edema dependent edema due to right-sided heart failure distended neck veins due to pulmonary hypertension enlarged, tender liver related to polycythemia and decreased cardiac output hepatojugular reflux (distention of the jugular vein induced by pressing over the liver) due to right-sided heart failure right upper quadrant discomfort due to liver involvement tachycardia due to decreased cardiac output and increasing hypoxia weakened pulses due to decreased cardiac output decreased cardiac output pansystolic murmur at the lower left sternal border with tricuspid insufficiency, which increases in intensity when the patient inhales. Complications Possible complications of cor pulmonale include: biventricular failure as the heart hypertrophies in an attempt to circulate the blood hepatomegaly edema ascites pleural effusions thromboembolism due to polycythemia.

Diagnosis The following tests help diagnose cor pulmonale: Pulmonary artery catheterization shows increased right ventricular and pulmonary artery pressures, resulting from increased pulmonary vascular resistance. Both right ventricular systolic and pulmonary artery systolic pressures are over 30 mm Hg, and pulmonary artery diastolic pressure is higher than 15 mm Hg. Echocardiography demonstrates right ventricular enlargement. Angiography shows right ventricular enlargement. Chest X-rays reveal large central pulmonary arteries and right ventricular enlargement. Arterial blood gas analysis detects decreased Pa O2 (usually less than 70 mm Hg and rarely more than 90 mm Hg). Electrocardiography shows arrhythmias, such as premature atrial and ventricular contractions and atrial fibrillation during severe hypoxia, and also right bundle branch block, right axis deviation, prominent P waves, and an inverted T wave in right precordial leads. Pulmonary function studies reflect underlying pulmonary disease. Magnetic resonance imaging measures right ventricular mass, wall thickness, and ejection fraction. Cardiac catheterization measures pulmonary vascular pressures. Laboratory testing may reveal hematocrit typically over 50%; serum hepatic tests may show an elevated level of aspartate aminotransferase levels with hepatic congestion and decreased liver function, and serum bilirubin levels may be elevated if liver dysfunction and hepatomegaly exist. Treatment Therapy of cor pulmonale has three aims: reducing hypoxemia and pulmonary vasoconstriction, increasing exercise tolerance, and correcting the underlying condition when possible. Treatment may involve: bed rest to reduce myocardial oxygen demands digoxin to increase the strength of contraction of the myocardium antibiotics to treat an underlying respiratory tract infection a potent pulmonary artery vasodilator, such as diazoxide, nitroprusside, or hydralazine, to reduce primary pulmonary hypertension continuous administration of low concentrations of oxygen to decrease pulmonary hypertension, polycythemia, and tachypnea mechanical ventilation to reduce the workload of breathing in the acute disease a low-sodium diet with restricted fluid to reduce edema phlebotomy to decrease excess red blood cell mass that occurs with polycythemia small doses of heparin to decrease the risk of thromboembolism tracheotomy, which may be required if the patient has an upper airway obstruction corticosteroids to treat vasculitis or an underlying autoimmune disorder.