37th Annual Advanced Practice in Primary and Acute Care Conference: October 9-11, 2014

SESSION FD3

8:30

Radiology Fundamentals: Shedding New Light on the Chest X-Ray Ronald Thompson, MD, MS Session Description: This presentation will benefit anyone who has a desire to understand the basic principles of Radiographic Imaging as related to chest x-rays. Utilizing radiographic images for diagnosing illness is an extremely useful tool in successfully managing patients, and has taken on increasing importance in recent years. Medical imaging has become an indispensable part of patient care, and the better clinicians are able to understand and utilize the basic principles and techniques of radiographic imaging, the more effective they can be in successfully treating their patients, and the more quickly their patients can be on the road to recovery. The lines and shadows on x-rays can be confusing. This presentation will help the attendee to look at and understand chest x-rays in a way that is logical and makes sense! Learning Objectives: Following my presentation, participants will be able to: 1. Identify basic principles that guide the interpretation of radiographic images. 2. State the different radiographic densities. 3. Discuss radiographic findings that distinguish normal chest anatomy from common chest diseases. 4. Describe the silhouette sign, understand its significance, and be able to apply in film analysis. 5. Recognize and discuss the meniscus sign. 6. Explain and recognize the difference between an uncomplicated pleural effusion and a malignant effusion. 7. Discuss the radiographic findings of congestive heart failure. 8. Discuss the radiographic findings of chronic obstructive pulmonary disease. 9. Explain and recognize the difference between volume loss and mass effect in the chest. 10. Discuss the importance of recognizing early volume loss in the chest. 11. Discuss the radiographic findings of lung cancer. 12. Recognize the importance of thinking through radiographic film analysis.

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RADIOLOGY FUNDAMENTALS: SHEDDING NEW LIGHT ON THE CHEST X-RAY

RADIOLOGY FUNDAMENTALS: CHEST IMAGING

Radiology Enterprises [email protected] www.radiologyenterprises.com 888-958-4804

Radiology Enterprises [email protected] www.radiologyenterprises.com 888-958-4804

CHEST IMAGING

RADIOGRAPHIC DENSITIES

Density Characteristics What are the different basic radiographic densities?

1. Metal 2. Bone (Calcification) 3. Soft Tissue 4. Fat 5. Air

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MENISCUS SIGN

MENISCUS SIGN RADIOGRAPHIC FEATURES • Smooth contour • Wedged shaped, reverse “V”, triangular • Lies along dependent portion of lung • Indicates UNCOMPLICATED fluid

PLEURAL EFFUSION

PLEURAL EFFUSION

GENERAL • A small amount of fluid is normally present to lubricate the surfaces of the pleura • A pleural effusion occurs when an excessive amount of fluid accumulates between the layers of tissue that line the lungs • At least 200-300 cc of fluid must be present before visible on an upright Chest X-Ray – Decubitus views of chest may show smaller amounts of fluid

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PLEURAL EFFUSION SYMPTOMS Chest pain Usually sharp Worse with cough or deep breath Dyspnea Cough Hiccups Tachypnea Shortness of breath Sometimes no symptoms

PLEURAL EFFUSION TRANSUDATE EXUDATE

PLEURAL EFFUSION • Different types of fluid can accumulate in the pleural space • Serous fluid (hydrothorax) • Blood (hemothorax) • Chyle (chylothorax) Occurs when thoracic duct is disrupted Lymphoma, trauma, thoracic surgery most common causes

• Pus (pyothorax or empyema)

PLEURAL EFFUSION TRANSUDATE – Caused by fluid leaking into the pleural space – Caused by systemic factors – Factors that alter the balance of formation and absorption of pleural fluid such as an increase in capillary hydrostatic pressure or a decrease in colloid oncotic pressure – Types of transudative pleural effusions • CHF • Cirrhosis

PLEURAL EFFUSION EXUDATE – Usually caused by pleural inflammation, infection, injury or lymphatic obstruction – Caused by alterations in local factors that influence formation and absorption of pleural fluid – Types of exudative pleural effusions • • • • • •

Bacterial pneumonia Cancer Pulmonary embolism Viral infection Trauma Collagen Vascular Disease – Rheumatoid Arthritis – Systemic Lupus Erythematosus

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PNEUMONIA

PNEUMONIA

Can be caused by a variety of agents Bacterial Viral Mycoplasma Fungi

PNEUMONIA

PNEUMONIA

An important cause of morbidity and mortality in the US Millions of cases reported yearly Accounts for over 1 mil hospitalizations Accounts for over 1 mil ER visits

VIRAL PNEUMONIA Approx 50% of pneumonias believed to be caused by viruses Generally less severe than those caused by bacteria Often seen in very young patients

PNEUMONIA

PNEUMONIA

BACTERIAL PNEUMONIA Pneumococcus most common cause Commonly called lobar pneumonia, even though infection does not usually involve the entire lobe Lower lobes and posterior segments of upper lobes most common

MYCOPLASMA PNEUMONIA Has features of both bacterial and viral pneumonias Usually causes a mild, wide spread infection Common cause of community acquired pneumonia

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PNEUMONIA

PNEUMONIA

SYMPTOMS

SYMPTOMS

Fever Cough Headache Muscle pain Weakness Fatigue SOB

Chills Chest pain Sweats Tachypnea Tachycardia Etc

PNEUMONIA

PNEUMONIA

RADIOGRAPHIC FINDINGS Patchy infiltrates Mottled infiltrates Peribronchial distribution Diffuse Homogeneous

RADIOGRAPHIC FINDINGS Focal alveolar infiltrates Interstitial densities Miliary, nodular, reticular With or w/o adenopathy

PNEUMONIA

PNEUMONIA

COMPLICATIONS Pleursy with effusion Empyema Pulmonary abscess Toxic ileus

COMPLICATIONS Rare: Broncopleural fistulas Pericarditis with effusion CHF

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CONGESTIVE HEART FAILURE

CONGESTIVE HEART FAILURE • • • • • •

Affects up to 5 million Americans 400,000 new cases each year 40,000 deaths a year Contributing factor in over 200,000 deaths Men > Women Blacks > Whites

CONGESTIVE HEART FAILURE Risk Factors • • • • • •

Smoking High Cholesterol Hypertension Diabetes Obesity CAD

CONGESTIVE HEART FAILURE KERLEY LINES -Radiographic Signs• Cardiac Enlargement • Enlarged Pulmonary Vasculature • Increased Interstitial Markings •Kerley B lines •Kerley A lines

• Pulmonary Edema • Pleural Effusions

• Named after Peter Kerley • Kerley A lines • Kerley B lines • Kerley C lines

•Blunting of CPA •If unilateral usually on right •If bilateral usually larger on right •If pt supine see homogeneous density over affected lung

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KERLEY LINES • Kerley B lines – – – – – – –

Short, parallel lines at lung periphery Represent dilatation of the interlobular septa 1-2 cm in length, usually less than 1 cm Parallel to one another At right angles to pleura Located peripherally Most often seen at lung bases • at costophrenic angles on PA radiographs • in substernal region on lateral radiographs

KERLEY LINES • Kerley C lines – Less commonly seen than any of the Kerley lines – Short, fine lines – Reticular in appearance – Seen throughout the lungs – Caused by • thickening of anastomotic lymphatics or • superimposition of many overlapping Kerley B lines

KERLEY LINES • Kerley A lines – Longer than Kerley B lines • at least 2cm in length or longer

– Located in inner half of lung – Oriented diagonally from lung periphery toward hila – Caused by distension of anastomotic channels between peripheral and central lymphatics of lung – Less commonly seen than Kerley B lines

KERLEY B LINES RADIOGRAPIC FINDINGS Thin linear lines 1-2 cm in length At lung bases At right angles to pleura Represent thickening of the interlobular septa Usually an indication of raised venous pressure Wall is normally hairline thin Often associated with: 1) Thickening of the fissures 2) Fluid in subpleural space 3) Pleural effusions

KERLEY B LINES CAUSES Congestive Heart Failure Mitral Stenosis Lymphangitic carcinomatosis Pulmonary fibrosis Parasitic infection Interstitial deposition of heavy metal particles

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COPD

COPD

CHRONIC OBSTRUCTIVE PULMONARY DISEASE Two most common conditions BRONCHITIS EMPHYSEMA Some think asthma should be included

CHRONIC OBSTRUCTIVE PULMONARY DISEASE Chronic Bronchitis Pts usually do not develop obstruction SX: cyanosis, edema of extremities, heart failure

COPD

COPD

CHRONIC OBSTRUCTIVE PULMONARY DISEASE Pulmonary Emphysema Permanent enlargement of air spaces distal to the terminal bronchioles

CHRONIC OBSTRUCTIVE PULMONARY DISEASE Pulmonary Emphysema Patients have difficulty breathing, with insufficient oxygen delivered to the blood

RADIOGRAPHIC FINDINGS OF COPD

RADIOGRAPHIC FINDINGS OF COPD

HYPERINFLATION OF LUNGS A-P diameter of chest increased Increase in size and lucency of retrosternal airspace Lungs are hyperlucent Localized bullae frequent

CHANGES IN PULM VESSELS Decrease in size and # of peripheral arteries Peripheral arteries thinned, tapered, and narrowed Central arteries prominent

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RADIOGRAPHIC FINDINGS OF COPD

RADIOGRAPHIC FINDINGS OF COPD

CHANGES IN PULM VESSELS Panlobular Empysema: lower lobes most involved, causing shunting of blood into upper lobes (cephalization)

CARDIAC CHANGES Cardio-mediastinal silhouette can become elongated and narrowed

RADIOGRAPHIC FINDINGS OF COPD

RADIOGRAPHIC FINDINGS OF COPD

DIAPHRAGMATIC CHANGES Diaphragms become low and flat In severe cases diaphragms may become inverted Diaphragm movement may become limited

CHEST X-RAY MAY BE COMPLETELY NORMAL

VOLUME LOSS AND MASS EFFECT

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RADIOGRAPHIC FINDINGS OF VOLUME LOSS ON CXR

VOLUME LOSS Ipsilateral structures shifted TOWARD the side of the abnormality

Heart, trachea, and mediastinum shifted toward the side of the abnormality Ipsilateral diaphragm elevated Contralateral lung overexpanded Ipsilateral lung smaller Contralateral rib spaces wider

Contralateral structures overexpanded

MASS EFFECT Occupies space All structures are pushed AWAY from the mass

LUNG CANCER

LUNG CANCER

• • • •

Most start in lining of the bronchi Thought to develop over many years Smoking is number one cause Most common cancer related cause of death • Over 200,000 new cases projected in US in 2014 • Over 160,000 deaths estimated

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LUNG CANCER • Accounts for about 28% of all cancer deaths • Black men about 40% more likely to develop lung cancer than white men • Rate about the same in black women and white women

RADIOGRAPHIC FINDINGS IN LUNG CANCER • • • • • • • •

Volume loss Unilateral enlargement of hilum Mediastinal widening Apical density w or w/o rib destruction Solitary pulmonary cavity Pneumonitis that does not clear Large parenchymal mass Solitary pulmonary nodule

LUNG CANCER SYMPTOMS • • • • • • • • •

Chronic cough Coughing up blood Wheezing Chest pain Hoarseness Weight loss Loss of appetite Shortness of breath Fever of unknown origin

RADIOGRAPHIC FINDINGS INDICATING METASTASIS OR LOCAL INVASION

• • • • •

Pleural effusion Lymphatic spread Hematogenous spread Pleural mass Diaphragmatic elevation

RADIOLOGY FUNDAMENTALS: CHEST IMAGING

Radiology Enterprises [email protected] www.radiologyenterprises.com 888-958-4804

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PLEURAL EFFUSION Pleural effusion is the most common sign of pleural pathology, caused by a mismatch in the rate of inflow and outflow within the pleural space. GENERAL CONSIDERATIONS: The pleura envelopes the lung with a serous membrane and contains a small amount of fluid which lubricates the pleural space, allowing the lungs to alter their shape and providing a cushion between the lungs and the chest wall. The parietal pleura is the portion of the pleura that lines the walls of the thoracic cavity including the ribs, diaphragm, and mediastinum. The visceral pleura is the portion of the pleura that lines the lungs and interlobar fissures, completely separating the different lobes. The visceral pleura lacks pain fibers and is relatively insensitive. The two pleural layers join together at the pulmonary hila and at the inferior pulmonary ligament. The anterior and posterior junction lines are formed where the two lungs contact each other and represents the interface of the right and left pleural surfaces of the thorax. FORMATION AND CAUSES OF PLEURAL EFFUSIONS: Pleural effusions are caused by: 1) 2) 3) 4) 5) 6)

Increased capillary hydrostatic osmotic pressure Decreased colloid osmotic pressure Increased microvascular permeability Decreased lymphatic pleural drainage Decreased pleural surface pressure Transdiaphragmatic passage of peritoneal fluid

Causes of pleural effusion include congestive heart failure, metastatic disease to the pleura, infections, pulmonary infarcts, tuberculous pruritus, pleural mesothelioma, systemic lupus erythematosus, nephrotic syndrome, pleural trauma, and Meigs syndrome. TRANSUDATES VERSUS EXUDATES: TRANSUDATES: Pleural fluid can be either a transudate or an exudate. Transudates result from decrease in colloid osmotic pressure and are caused by disease states that cause hyponatremia. Transudates can also result from increased microvascular hydrostatic osmotic pressure. With transudative fluid, the pleura is normal. Congestive heart failure is the most common cause, with other less common causes including cirrhosis, nephrotic syndrome, nephrogenic effusion, hypoalbuminemia, constrictive pericarditis, atelectasis, pulmonary embolus, and myxedema. Transudates are often bilateral. EXUDATES: Pleural effusions which are exudates result from an alteration in the pleural surface from increased permeability or decrease in lymphatic flow, usually secondary to pleural malignancy or inflammatory conditions. When the ratio of pleural fluid to serum protein is greater than 0.5, or when the ratio of pleural fluid to serum LDH is greater than 0.6, exudative fluid can be established.

RADIOGRAPHIC APPEARANCE: The earliest finding of a small effusion on the chest x-ray is blunting of the costophrenic angle (CPA). The fluid first collects here because this is the most dependent portion of the lung when the patient is upright. The CPA, which usually has a sharp angle, becomes blunted with an upward, concave border. At least 200 cc of fluid is needed to blunt the CPA on an upright PA chest, and at times up to 500 cc may not be apparent. The most sensitive radiographic projection to detect small amounts of fluid is the lateral decubitus view. The appearance of the fluid will depend on the position of the patient and on the mobility of the fluid. 1) LARGE PLEURAL EFFUSIONS: These effusions are of homogeneous density, and are located in the dependent portion of the chest. Their lateral border forms a meniscus, which is a crescentic, curvilinear upper lateral border. Effusions located at the lung bases obscure the diaphragm (silhouette sign), and if the fluid is adjacent to the heart border that will also be obscured (silhouette sign). In massive effusions, there can be widening of the interspaces of the ribs and contralateral displacement of the heart and mediastinum. The fluid may also extend into the fissures of the lung, resulting in enlargement and distention. 2) PLEURAL EFFUSIONS IN SUPINE PATIENTS: With the patient supine, the effusions layer posteriorly, creating a hazy density over the entire hemithorax affected. It is possible to miss large effusions in supine patients because of the posterior layering of the effusions. Generally, the volume of fluid is underestimated when the patient is supine. As the fluid flows into the apices of the lung, there can be "capping" of the lung apices. This can be used as an early sign of pleural fluid in a supine patient because the apex of the lung is the most dependent portion of the thorax when the patient is in a supine position. The paraspinal soft tissues will be widened when the effusions are large and there can also be thickening of the interlobar fissures. 3) SUBPULMONIC EFFUSIONS: Subpulmonic effusions occur when fluid collects between the diaphragm and the inferior surface of a lower lobe. This may simulate an elevated hemidiaphragm. When unilateral, subpulmonic effusions are more common on the right side. Bilateral, subpulmonic effusions may be overlooked, giving the appearance of apparently bilaterally elevated diaphragms. The superior margin of the fluid collection mimics the contour of the diaphragm, resulting in the appearance of an elevated ipsilateral diaphragm, however, there is flattening of the medial portion of the diaphragm, and the dome of the diaphragm appears shifted laterally. These are signs which can be used to differentiate a subpulmonic effusion from a truly elevated diaphragm. Also, blunting of the CPAs is a valuable clue for detection of subpulmonic effusions. When the subpulmonic effusion is on the left side, an increased distance between the gastric fundus and the leaf of the "diaphragm" can be another clue to the diagnosis. When a subpulmonic effusion is suspected, a lateral decubitus view can be very helpful in demonstrating the presence and amount of fluid and will also help to show the true position of the diaphragms. This can be helpful if volume loss is a consideration as the reason as to why the diaphragm is elevated. 4) LOCULATED PLEURAL EFFUS IONS. Loculated pleural effusions are accumulations of pleural fluid within the fissures or between the visceral and parietal pleura when the pleural layers are adherent due to scarring, fibrosis, adhesions, or other factors which . restrict movement, preventing the fluid from freely shifting in the pleural space.

Location of loculated effusions: Loculated fluid occurs between the lung and chest wall or in interlobar fissures. They are often posterior, commonly forming adjacent to the chest wall, but can be anywhere. Appearance of loculated effusions: Loculated effusions usually appear as a circumscribed, homogeneous peripheral density, which, at times, if within an interlobular fissure, may simulate a tumor mass in the frontal view, but on the lateral view the density conforms to the location and direction of the fissure. Air fluid levels can appear, and often occur after thoracentesis has been performed, or can be seen if there is a broncho-pleural fistula or if a gas producing organism is present. To differentiate free fluid from loculated fluid, films with the patient in different positions should be obtained.

PNEUMONIA Pneumonia encompasses many different diseases that cause infection or inflammation in the lungs. It can be caused by a variety of agents, including bacteria, viruses, mycoplasmas, fungi, and others. FACTS AND FIGURES:

Pneumonia is an important cause of morbidity and mortality in the United States, with millions of cases reported yearly. It accounts for over 1,000,000 hospitalizations and over 1,000,000 emergency room visits. TYPES OF PNEUMONIA:

The types of pneumonia include viral pneumonia, bacterial pneumonia, and mycoplasma pneumonia. Other, less common types, include Pneumocystis carinii pneumonia, which is caused by a fungus, predominantly seen in patients with AIDS, chemical pneumonia, Legionella pneumonia, eosinophilic pneumonia, and necrotizing pneumonia. Pneumonia can also be caused by inhalation of food, liquids, gases, dust, or fungi. VIRAL PNEUMONIA:

Approximately 50% of pneumonia cases are believed to be caused by viruses. This type of pneumonia is generally less severe than those caused by bacteria, with symptoms produced similar to those in patients that have influenza, including fever, dry cough, headache, muscle pain, weakness, and increasing breathlessness. This type of pneumonia is often seen in very young patients. BACTERIAL PNEUMONIA:

Pneumococcus is the most common cause. This type pneumonia is commonly called lobar pneumonia, even though the infection does not usually involve an entire lobe. The lower lobes and posterior segments of the upper lobes are most commonly involved. Bacterial pneumonia can cause serious harm in otherwise healthy people, especially when the body's defenses are weakened. It is a common cause of community-acquired pneumonia. The onset varies from gradual to sudden and the symptoms include fever, shaking, chills, chest pain, fatigue, sweats, productive cough, shortness of breath, tachypnea, and tachycardia. MYCOPLASMA PNEUMONIA:

This type of pneumonia has characteristics of both bacterial and viral pneumonia, and usually causes a mild and wide spread infection. The most prominent symptom is cough, which tends to come in violent attacks. Only a small amount of sparse whitish sputum is characteristically produced. It is a common cause of community-acquired pneumonia in otherwise healthy individuals below 40 years of age, with the highest rate in patients between 5 to 20 years.

RADIOGRAPHIC FINDINGS OF PNEUMONIA ADENOVIRAL INFECTIONS: Severe upper respiratory symptoms are often due to adenovirus infections, and even though severe, they often produce no x-ray changes. If pneumonia does develop, typically patchy infiltrates are seen which can be mottled in the peribronchial regions or can be diffuse, homogeneous densities. In most cases, systemic adenopathy is present and hilar adenopathy is also common. In children there may be a diffuse bilateral bronchopneumonia with pronounced hyperinflation of the lungs. Chronic sequelae such as bronchiectasis and unilateral hyperlucent lung can occur (Swyer-James syndrome). This type of pneumonia is unusual in adults, and although the pulmonary involvement may be extreme as viewed on the chest x-ray, the acute illness may not be severe. Resolution usually occurs slowly. The most common infiltrates seen on the chest x-ray are widely scattered patchy or confluent densities, usually in a peribronchial distribution. VIRAL PNEUMONIA:

A wide variety of appearances can be seen on the chest x-ray, with viral pneumonias, usually including focal alveolar infiltrates or interstitial densities. Other patterns include miliary, nodular or reticular infiltrates, or diffuse perihilar densities. Pleural reaction is rare, and in children a bilateral lower lobe predilection is common. Hilar nodes are enlarged and the chest x-ray may be normal for several days after the onset of symptoms, and when changes on the chest x-ray do occur, they may persist for days or weeks after the patient has clinically recovered. PNEUMOCOCCAL PNEUMONIA: This type pneumonia results in an alveolar or air space pneumonia with a predilection for basilar segments and posterior segments of the lung. The onset of symptoms is usually sudden with the infiltrate on the CXR beginning peripherally and spreading centrally. The usual appearance is a homogeneous dense consolidation of a lower lobar segment. The density commonly extends to the pleural surface. Air bronchograms are commonly seen and represent fluid or exudates in the alveoli. A mild degree of atelectasis may also be seen due to bronchial involvement and obstruction. During resolution the density becomes mottled, scattered, patchy, and irregular in contrast to its homogeneous appearance earlier in the disease process. The infiltrate usually clears completely in one to three months. COMPLICATIONS OF PNEUMOCOCCAL PNEUMONIA:

1) Pleurisy with effusion: The commonest complication. Occurs in less than 10% of cases. 2) Empyema Occurs in less than 2% of patients. The thick empyemic fluid has a tendency to loculate, forming circumscribed densities with a convex central border. Resolution is slow. If persistent, pleural calcification may develop.

3) Pulmonary Abscess: Fortunately, is now a rare complication of pneumonia. Initially abscess appears as a circumscribed density as the pneumonia resolves. If abscess extends into a bronchus, air fluid levels may occur. 4) Toxic Ileus: Dilated loops of bowel can be seen along with a distended abdomen. 5) Rarer Complications: Bronchopleural fistulas, pericarditis with effusion, acute gastric dilatation, congestive heart failure. MYCOPLASMA PNEUMONIA:

Mycoplasma pneumonia may cause up to 50% of all pneumonias in children less than 16 years of age. It typically occurs in young, otherwise healthy adults and, if acute, is usually mild and self limited in most cases, but may be severe with wide spread pulmonary disease. The onset of symptoms is usually gradual, and the radiographic features may be delayed for two to three days after symptoms begin. Typically, a large variety of infiltrates may occur, with the infiltrates having no particular distinguishing features from viral or pneumococcal pneumonias. The distribution may be segmental or lobar, but can also be interstitial with a reticulonodular or mixed pattern. There is a tendency for the disease to clear in one area and spread in another area, often the opposite lung. In one half of the patients the infiltrates are bilateral and have a predilection for lower lobes. The infiltrates typically are patchy, and there may be a nodular or reticular pattern. Atelectasis may occur and hilar adenopathy is frequent. Pneumatoceles may occasionally form. Pleural reaction, which is common in children, is unusual in adults. They tend to resolve slowly, often persisting for several weeks after the clinical symptoms have disappeared.

CONGESTIVE HEART FAILURE Congestive heart failure is a serious condition. As the name implies, congestive heart failure results in congestion of the heart, congestion of the lungs, congestion of the pulmonary vasculature, and congestion of the tissues of the body. The heart does not actually "fail", but is unable to pump enough blood to meet the body's needs, and as a result the blood backs up in the heart and in structures proximal to the heart, resulting in "congestion". Congestive heart failure effects almost five million Americans, and usually develops gradually, over a number of years, resulting in the heart inefficiently pumping blood to the remainder of the body. Because the heart loses its pumping efficiency, circulation is poor, and this leads to blood backing up in the veins. The fluid in the veins eventually seeps out, causing congestion in the surrounding tissues. Excessive fluid tends to build up, especially in the lower legs and ankles, causing swelling or edema. Conditions which result in heart problems that can lead to congestive heart failure include coronary artery disease and high blood pressure. How serious the condition is depends on how much of the heart's pumping capacity has been lost. As the condition worsens, less and less blood can get to other vital organs such as the brain, lungs, and kidneys, causing these organs to function poorly. The kidneys become compromised in their ability to eliminate the body of sodium and water which leads to retained water and edema in the body tissues. The heart tries to compensate for its decreased pumping ability by enlarging or dilating which allows more blood to flow into the heart. The muscle fibers of the heart thicken or hypertrophy, which allows the heart to contract more forcefully, and therefore pump more blood. The heart also tries to compensate by contracting more frequently (tachycardia) in order to increase the amount of blood into the circulation. By these three methods the heart can temporarily compensate for its loss of pumping efficiency, sometimes for years, but compensation has it limits, and eventually signs of heart failure will appear. Heart failure has been divided into several types as described below: RIGHT HEART FAILURE OR DIASTOLIC HEART FAILURE: In this type of failure the heart has a problem relaxing, and cannot properly fill with blood because the muscle has become stiff. There is a backup of fluid proximal to the heart, in the venous side of the circulation, resulting in fluid congestion in the veins, with the fluid eventually seeping out, causing the surrounding tissues to become congested with excessive build up of fluid, often in the lower legs and ankles resulting in swelling and edema. This situation may lead to weight gain which is one of the symptoms of congestive heart failure. Also, because of the congestion, the patient feels tired, and because the body tissues are not receiving adequate oxygenated blood, tiredness and decreased exercise ability is common. LEFT HEART FAILURE OR SYSTOLIC HEART FAILURE: With systolic heart failure, the heart's ability to contract is compromised and the heart cannot pump with enough force to furnish sufficient amounts of blood into the circulation to supply vital organs. There is excessive backup of blood into the lungs which starts to leak out, resulting in a condition known as pulmonary congestion, characterized by excessive fluid in the lungs and excessive fluid in the pulmonary vessels. Fluid builds up in the interstitium of the lungs, and eventually builds up in the alveoli, resulting in pulmonary edema. In this setting patients experience difficulty breathing, weakness, disrupted sleep patterns, fatigue, and easy tiring. Without the proper "fuel" being provided to the muscles and other tissues, the body cannot perform its work properly leading to tiredness, malaise, easy fatigue, and decreased exercise tolerance.

CAUSES OF CONGESTIVE HEART FAILURE: Nearly everyone loses some pumping ability and pumping efficiency of their heart with age, but the loss is much more in patients with heart failure and is often caused and exacerbated by other diseases that can damage the heart such as hypertension, narrowing of the arteries supplying blood to the heart (coronary artery disease), diabetes, inflammatory conditions, infectious conditions such as endocarditis and myocarditis, alcohol, chemotherapy, and valvular heart disease. FACTS AND FIGURES ABOUT CHF: Up to five million Americans have congestive heart failure, with approximately four hundred thousand new cases diagnosed every year, with the condition being slightly more prominent in men than women, and two times as common in blacks than whites. Congestive heart failure is a contributing factor in over 225,000 deaths in the U.S. Heart failure mortality is twice as high for blacks than whites. The risks of congestive heart failure increase with age. Congestive heart failure is closely associated with the major risk factors for coronary artery disease, including smoking, high cholesterol levels, hypertension, diabetes, and obesity. Diabetes and hypertension are particularly important, with uncontrolled high blood pressure increasing the risk of CHF by 200% compared to those who do not have hypertension, and patients with diabetes having a two to eight times greater risk of CHF compared to those who do not have diabetes. The presence of coronary artery disease is among the greatest risk factors for developing CHF. RADIOGRAPHIC SIGNS OF CONGESTIVE HEART FAILURE: 1) CARDIAC ENLARGEMENT: The transverse diameter of the heart usually increases. 2) DILATATION OF THE PULMONARY VASCULATURE: The pulmonary vessels become engorged and distended, with the individual vessels appearing blurred and less distinct than normal, findings indicating perivascular edema. The vessels become redistributed, with the upper lobe vessels appearing larger than the lower lobe vessels (cephalization). 3) INCREASED INTERSTITIAL MARKINGS: As fluid accumulates in the interstitial structures of the lungs, Kerley A and B lines can be seen. KERLEY B LINES: These lines represent dilatation of the interlobular septa which becomes thickened by fluid. These are small, dense, horizontal lines that measure up to 2 cm in length, usually best seen along the lateral periphery of the lower lobes. KERLEY A LINES: These lines are longer, ranging in size from 5 to 10 cm, and usually are straight or slightly curvilinear, extending from the hilar regions toward the periphery of the lungs. They are usually seen in the upper lobes as opposed to Kerley B lines which are usually seen in the lower lobes. These lines also represent fluid in the interlobular septa. 4) PULMONARY EDEMA: In pulmonary edema, also referred to as alveolar edema, there is leakage of fluid into the alveoli of the lungs, resulting in diffuse, fluffy opacities in the lungs, often bilateral, and usually in the perihilar region, causing a typical "bat wing" pattern. Rarely pulmonary edema can be unilateral. 5) PLEURAL EFFUSIONS: Pleural effusions can also occur. These are usually basal densities that obliterate the costophrenic angles and obscure the contour of the diaphragms. The fluid may extend into the interlobular fissures. When effusions are unilateral, they are usually on the right side, and if bilateral, are usually larger on the right side. If the patient is supine, the effusion may appear as a homogeneous density over the entire portion of the affected lung.

CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD) Chronic obstructive pulmonary disease refers to a large group of lung diseases, the two most common of which are chronic bronchitis and emphysema. These lung diseases interfere with the patient's breathing. It is estimated that eleven percent of the U.S. population has COPD with the incidence increasing. CHRONIC BRONCHITIS: Patients who have chronic bronchitis usually do not develop obstruction, but fifteen percent of patients do. These patients will experience such symptoms as cyanosis, edema of the extremities, and heart failure. PULMONARY EMPHYSEMA: Pulmonary emphysema is a chronic lung disease which is defined by the National Heart, Lung, and Blood Institute as abnormal permanent enlargement of the air spaces distal to the terminal bronchioles, with associated destruction of the alveolar walls, without areas of obvious fibrosis. These abnormally enlarged air spaces trap "stale" air, and do not effectively exchange it with fresh air, resulting in difficulty breathing and in insufficient oxygen being delivered to the blood. This process results from irreparable damage to the pulmonary septal tissue which is distal to the terminal non-respiratory bronchiole. In this setting, abnormally enlarged air spaces replace normal lung tissue and it is this feature of the disease which accounts for many of the changes which are seen on the chest x-ray, both directly and indirectly. Pulmonary emphysema is seen most commonly in heavy smokers. A hereditary form of the disease, Alpha I Antitrypsin Deficiency, is a relatively uncommon form of severe emphysema, occurring in young people, usually under forty years of age, predominantly effecting the lower lobes. SUB TYPES OF PULMONARY EMPHYSEMA:

1) CENTRILOBULAR: This is the most common form of pulmonary emphysema which is strongly associated with heavy smoking. The severity of the emphysema is proportional to the number of cigarettes smoked. It has mainly an upper lobar distribution, and is caused by destruction of the alveoli around the proximal respiratory bronchioles. 2) PANLOBULAR EMPHYSEMA: This type of emphysema has a characteristic lower lobe distribution in which the alveoli are destroyed throughout the secondary pulmonary lobule. This is the type of emphysema seen in patients with Alpha I Antitrypsin Deficiency. 3) PARA SEPTAL EMPHYSEMA: This type of emphysema can be either focal or multi-focal, and involves the periphery of the lobule, leading to formation of bullae. Bullae are air filled sacs which are greater than 1 cm, with thin walls which can become so large as to replace an entire lobe. Occasionally a bulla will rupture and produce a condition called pneumothorax. The absence of normal lung markings is striking when large bullae are present. 4) PARACICATRICIAL EMPHYSEMA: A fourth type of emphysema, paracicatricial, is associated with pulmonary fibrosis, and therefore does not meet the strict definition of emphysema.

SYMPTOMS: Emphysema is found at autopsy in up to 66% of adult patients, but clinical detection of the disease during life is difficult unless the condition is severe. Patients with emphysema typically exhibit cough, progressive difficulty breathing, air flow obstruction, reduction in maximal expiratory flow rate, increased residual volume, and impairment of gas transfer as measured by carbon monoxide diffusing capacity SIGNS: In chronic bronchitis, initially the patient may look normal, however, with time the lips and skin become cyanotic, abnormal lung sounds occur, as well as swelling of the feet, and eventual heart failure. In pulmonary emphysema the patients usually do not become cyanotic, but eventually appear underweight with shortness of breath a predominant symptom. The chest may increase in size from front to back (the socalled barrel chest) and the lung sounds may be diminished. ROENTENOGRAPHIC FINDINGS: Accuracy of diagnosis on chest x-ray depends on the severity of the parenchymal destructive changes and ranges from 65% to 80%. CT is the best way of recognizing pulmonary emphysema, but even CT underestimates the disease as compared to pathologic assessment. On chest x-ray the following findings are observed: 1)

Hyperinflation of the lungs:

The anterior - posterior diameter of the chest is increased. There is an increase in size and lucency of the retrosternal air space. The lung fields are hyperlucent. Localized bullae are frequent.

2)

Changes seen in the pulmonary vessels:

There is a decrease in the number and size of the peripheral arteries (peripheral vascular attenuation). In panlobular emphysema the lower lobes are most involved which can cause shunting of the blood into the upper lobes (cephalization). The central pulmonary arteries are prominent. The peripheral arteries become thinned, tapered and narrowed.

3)

Cardiac changes:

The cardio-mediastinal silhouette is elongated and narrowed. Cor pulmonale can develop, and if this happens the right ventricle becomes enlarged.

4)

Diaphragmatic changes:

The diaphragms become low and flat. In severe cases the diaphragms may become inverted. There is limitation of diaphragmatic movement to less than 2 cm as seen under fluoroscopy. 5)

It is not uncommon that the chest x-ray is completely normal in patients with mild to moderate pulmonary emphysema.

ALPHA 1 ANTITRYPSIN DEFICIENCY:

This is a hereditary condition, usually occurring in patients younger than 40 years of age resulting in severe pulmonary emphysema, predominantly effecting the lower lobes. These patients have a high incidence of liver cirrhosis and a high incidence of primary hepatoma.