Central venous catheters, often referred to as CVP (central venous pressure) lines, are used to monitor CVP and administer fluids intravenously. A centrally placed catheter ensures more consistent venous flow than does a route through the peripheral veins, which may vasoconstrict, particularly during periods of cardiovascular collapse. The internal jugular, subclavian, and femoral veins constitute the three most common access sites for CVP catheter placement.

The origins of the brachiocephalic veins (BCV) are demarcated by the sternoclavicular joint. Catheters within the left BCV show an anterior curve on the lateral chest radiograph because the left BCV crosses anteriorly to join the right BCV (Fig. 5-1). The subclavian veins drain the upper extremities and are a continuation of the axillary veins at a point demarcated by the lateral aspect of the first rib. The internal and external jugular and vertebral veins also contribute to the origin of each BCV. The left superior intercostal vein drains the second through fourth posterior intercostal veins and arches anteriorly to join the left BCV. It courses along the aortic arch, occasionally forming a rounded projection on the frontal chest radiograph referred to as the "aortic nipple."

The preferred position of a CVP line tip is central to the venous valves, at the origin of the superior vena cava (SVC). The SVC is formed by the junction of the right and left BCVs. This junction lies to the right of midline at the level of the first intercostal space. The SVC is the preferred location for measuring CVP and avoiding catheter complications. The SVC is joined by the azygos vein posteriorly, just prior to entering the pericardium. Posterior orientation of the catheter tip suggests that it enters the azygos vein (Fig. 5-2).

Peripherally inserted central catheters (PICCs) are small-caliber tubes that can be left in place for long durations. The preferred position of these catheters is reported to be the SVC (1,2); however, at some institutions, these catheters are placed in the radiology department, under direct fluoroscopic guidance, into the right atrium. There is little or no risk of atrial rupture or dysrhythmia with this placement, and there is a decreased incidence of peritip thrombus, which occurs with SVC placement in up to 90% of patients (3).

A left-sided SVC, a normal anatomic variant, is found in 0.3% of normal individuals (Fig. 5-3). Eighty percent of such patients also have a right-sided SVC and 60% have a left BCV connecting the right and left SVCs (4). When a left SVC is present, both the right SVC and the left BCV are usually diminutive. The left SVC most commonly drains into the right atrium via a dilated coronary sinus.

Many potential complications of CVP catheter placement can be recognized on chest radiography (Table 5-1). As many as one third of CVP catheters are placed incorrectly at the time of initial insertion (5) (Figs. 5-4 and 5-5). The most common
aberrant locations include the internal jugular vein, the right atrium or ventricle, the opposite subclavian vein, the corresponding artery, the inferior vena cava, and various extrathoracic locations. Placement within the right atrium can lead to cardiac perforation by the catheter (although this is less of a risk with some of the commonly used, peripherally placed, flexible, small-bore PICC lines) (6). Positioning in the area of the tricuspid valve can cause dysrhythmias. Aberrant positioning will interfere with accurate measurement of central venous pressure and can lead to infusion of potentially toxic substances directly into the liver or heart rather than into the central venous system, where rapid dilution can take place. Catheter tips that are directed against the lateral wall of the SVC can produce excess focal pressure on the venous wall, leading (although rarely) to venous perforation (7).

Pneumothorax occurs with 6% of CVP catheter placements (8). In evaluating for pneumothorax, the entire pleural surface should be evaluated bilaterally, since a failed attempt at placement of a CVP catheter on one side may have gone undetected clinically before successful placement on the opposite side. Every chest radiograph should be evaluated for pneumothorax when a CVP catheter is present. This is because the initial radiograph, especially if supine, may not demonstrate the pneumothorax, and pneumothorax can persist several days after
line placement (9). Skin folds, commonly seen on supine chest radiographs, may produce a thin radiopaque line that mimics a pneumothorax. Repeating the exam after repositioning the patient usually solves the dilemma.

Also occurring with CVP catheters placed via the subclavian vein is the complication of ectopic infusion of fluid into the mediastinum or pleural space (10) (Fig. 5-6). The rapid accumulation of fluid opacifying the mediastinum or pleural space after insertion of a subclavian catheter should suggest the diagnosis of ectopic infusion, which can be confirmed by injection of contrast through the catheter or thoracentesis if the fluid is accumulating in the pleural space.

Laceration of the catheter by the insertion needle, catheter fracture at a point of stress, or detachment of the catheter from its hub can result in catheter embolization. The catheter fragment can lodge in the SVC, inferior vena cava, right side of the heart, or pulmonary artery and can cause thrombosis, infection, or perforation (11).

Inadvertent puncture of the subclavian artery during subclavian vein CVP catheter placement can result in localized bleeding, which may be self-limiting but is rarely severe enough to require surgical intervention (Figs. 5-7 and 5-8). Air embolization can occur during venipuncture or intravenous contrast injection. When this occurs, air may be visible in the pulmonary artery on a chest radiograph or computed tomographic (CT) scan, signifying this usually asymptomatic but potentially fatal complication. Clot frequently forms around the catheter tip with prolonged catheter placement, resulting in malfunctioning of the catheter. If thrombus progresses, venous occlusion and even pulmonary embolus can result. "Pinch-off" syndrome refers to compression of a CVP catheter between the clavicle and the first rib. This compression can lead to catheter fracture or fragmentation (12).

Pulmonary artery catheters consist of a central channel to monitor left atrial pressure and a second channel connected to
an inflatable balloon at the catheter tip (13). A third channel measures CVP and cardiac output. The catheter is usually inserted from a subclavian vein approach, but jugular and femoral vein approaches are also used through a sheath called a cordis. The sheath allows easy advancement and withdrawal of the catheter and serves as short-term venous access after the pulmonary artery catheter has been removed. The purpose of the pulmonary artery catheter is to measure pulmonary capillary wedge pressure, which reflects left atrial pressure and left ventricular end-diastolic volume. Measurements of pulmonary capillary wedge pressure help to differentiate cardiogenic from noncardiogenic pulmonary edema. The ideal catheter tip position is within the right or left pulmonary artery or within the proximal interlobar artery. Inflation of the balloon causes the catheter to float into a peripheral pulmonary artery branch, in a wedged position, and deflation of the balloon results in the catheter resuming its more central position.

An important complication associated with the pulmonary artery catheter is pulmonary infarction distal to the catheter tip (14). This occurs when the catheter tip is placed too distally within the pulmonary artery. As the diameter of the catheter approaches the diameter of the pulmonary artery in which the catheter resides, occlusion of the artery by the catheter occurs. Clot can also form around the tip of the catheter and occlude the pulmonary artery, occasionally leading to pulmonary infarction (seen as patchy airspace opacification, often wedge shaped and in a subpleural location).

The pulmonary artery catheter balloon appears radiographically as a 1-cm rounded radiolucency at the tip of the catheter (Fig. 5-9). The balloon should be inflated for only a very short period of time, during measurement of pressure, and it should not be inflated while chest radiography is performed. If the balloon is left inflated, it can obstruct a major pulmonary artery and lead to pulmonary infarction.

Coiling or redundancy of pulmonary artery catheter tubing in the right side of the heart can irritate the myocardial conduction bundle and result in dysrhythmias (Fig. 5-10). Other potential complications of pulmonary artery catheter placement
include pulmonary artery rupture (leading to pulmonary hemorrhage), pulmonary artery pseudoaneurysm (Figs. 5-11 and 5-12), fistulae between the pulmonary artery and the bronchial tree, intracardiac knotting of the catheter, and balloon rupture (Table 5-2). Complications that can occur with CVP catheter placement can also occur with pulmonary artery catheter placement (Fig. 5-13).

The intra-aortic balloon pump (IABP) (also called an intra-aortic counterpulsation balloon) is used in some centers to improve cardiac function in the setting of cardiogenic shock. The device consists of a long inflatable balloon (26 to 28 cm in length) that surrounds the distal end of a centrally placed catheter. The catheter is placed via a femoral artery retrograde to the thoracic aorta. The balloon is inflated during diastole (increasing diastolic pressure to the coronary arteries and increasing oxygen delivery to the myocardium) and is forcibly deflated during systole (decreasing left ventricular afterload and oxygen requirements). A commonly used IABP is radiolucent, except for a radiopaque marker that defines its tip. The balloon can be seen as a long tubular radiolucency (Fig. 5-14), following the expected course of the descending thoracic aorta to the left of the thoracic spine, if the radiograph is exposed during diastole when the balloon is inflated. The ideal location of the tip is just distal to the left subclavian artery (projecting at the level of the aortic arch on a frontal chest radiograph), allowing maximal augmentation of diastolic pressures in the proximal aorta. Even with appropriate positioning, the mesenteric and renal artery ostia are crossed by the long balloon (15). If the IABP is advanced too far, it may obstruct the left subclavian artery (Fig. 5-15) or cause cerebral embolus. If the IABP is not advanced far enough, less effective counterpulsation can result (Fig. 5-16).

Aortic dissection can occur during IABP insertion, which may result in death (16). Other potential complications include reduction of platelets, red blood cell destruction, peripheral emboli, balloon rupture with gas embolus, renal failure, and vascular insufficiency of the catheterized limb (17) (Table 5-3).

Ventricular assist devices (VADs) are surgically implanted mechanical devices used in some medical centers to perform the work of the right (RVAD), left (LVAD), or bilateral (BVAD) ventricles in patients with intractable congestive heart failure. VADs can be implanted to support the failing heart and serve as a “bridge to transplant.” In some patients with reversible
forms of cardiac failure, a VAD can be implanted with the hope that it will allow the heart to recover; the assist device can be removed later. This indication is known as "bridge to recovery" (18). In selected patients who are not good candidates for cardiac transplantation because of other medical complications, VADs can be implanted as a means of supporting circulation over a period of years. This indication is known as "destination therapy." The new generation of pumps is designed for chronic, out-of-hospital use so that most patients can return home after the VAD is implanted. Reported complications from VAD placement, recognized on chest radiographs and CT scans, include pneumothorax, hemothorax, infection, thromboembolism, bowel obstruction, and mechanical failure (19). On chest radiography, the TCI Heartmate LVAD pump (Thermocardiosystems Inc., Woburn, MA) is identified in the left upper quadrant of the abdomen. The inflow cannula of the pump inserts into the left ventricular apex, directed at the mitral valve, drawing blood from the heart into the pump, and the polymer graft outflow cannula, usually 12 to 15 cm in length, carries blood from the pump to the ascending aorta (Fig. 5-17). Much of the outflow cannula is radiolucent. The inflow and outflow conduits contain porcine bioprosthetic valves, which are located outside the pump. A drive line, which exits through a fascial tunnel in the left lower quadrant of the abdomen, connects the device to an external portable console, which provides either pneumatic or electric power to the device.

Numerous types of single- and dual-lead pacemakers and combination pacer–defibrillators are available. They are used to treat a variety of dysrhythmias. Accurate interpretation of their appearance on chest radiography requires knowledge of the specific type of pacemaker placed. The three major approaches to insertion of a pacemaker electrode into the heart include epicardial, subxiphoid, and transvenous implantations; transvenous is the most common. With single-lead pacers, the wire is placed into the right ventricle by way of the cephalic, subclavian, or jugular vein. When the lead is wedged into the myocardial trabeculae near the cardiac apex, the lead will be stable and have maximal contact with the endocardial surface. With dual-lead pacers, one lead is generally placed into the right atrium and the other into the right ventricle. It is important to know where the desired placement of leads is for each patient, because placement within the coronary sinus may be accidental or purposeful. After the electrodes are positioned, the generator is placed in a pouch in the subcutaneous tissues of the chest wall or beneath the pectoralis muscle. Biventricular pacemakers are used to treat congestive heart failure. Leads are placed in the right atrium and right ventricle, and a third lead is placed in the coronary sinus for pacing the left ventricle (Fig. 5-18).

Failure of the pacemaker to elicit a ventricular response may be caused by (a) exit block, (b) lead fracture, (c) electrode dislodgment, (d) electrode malposition, (e) myocardial perforation, (f) thrombosis, (g) infection, or (h) battery failure (20). Of these, malpositioning, fracture, and perforation may be recognized on chest radiographs. The leads can be malpositioned within the coronary sinus, and in this case the catheter often appears to be ideally positioned on the frontal radiograph but
is directed posteriorly rather than anteriorly on the lateral projection. Approximately 2.7% of electrodes will fracture (21), generally near the pulse generator, at sharp bends in the lead wires, at the point of venous entry, or where the lead is embedded in the cardiac muscle (Figs. 5-19, 5-20, 5-21). If the insulating sheath holds the ends of a fractured lead in close proximity, the fracture may not be readily visible on a radiograph. Tight anchoring ligatures at the venous entry site can produce lucency of the lead, giving the false appearance of a fracture.

Electrode dislodgment occurs in 3% to 14% of patients (22), generally during the first weeks following insertion. Late displacement is uncommon because of the fibrin sheath that develops between the electrode and the endocardium. Twiddler's syndrome is a rare complication seen in patients with implanted pacemakers or defibrillators; it is a result of the patient either consciously or unconsciously twisting and rotating the implanted device in its pocket, resulting in torsion, dislodgment, and often fracture of the implanted lead (23,24). The diagnosis is confirmed by a chest radiograph, which will reveal a twisted, entangled, and dislodged pacing lead. A small amount of catheter play should be present during systole, but
none should be present during diastole. If the catheter is short, dislodgment may occur, and the catheter may enter the right atrium, pulmonary artery, SVC, or coronary sinus. If the lead is too long, a bend in the wire may occur, causing lead fracture (Fig. 5-22). A redundant lead may also perforate the myocardium; this complication generally occurs at the time of or within a few days after insertion. The frontal or lateral radiograph will show the catheter tip outside or within 3 mm of the edge of the cardiac silhouette (Fig. 5-23). Perforation can lead to cardiac tamponade or postcardiotomy syndrome. Inflammation and infection can occur within the vein or the generator pocket; the latter occurs in up to 5% of patients (20). Major vein thrombosis and pulmonary embolism are additional complications of pacemaker insertion.

There are several models of implantable cardioverter-defibrillators, which are used for treatment of life-threatening ventricular tachyarrhythmia, generally using a combination of two transvenously placed electrodes and one subcutaneous electrode. A thoracotomy may or may not be required for placement, although most are now placed transvenously. These devices can be combined with a preexisting pacemaker. It is important that the radiologist be familiar with the normal appearance, variations, and complications of these devices, such
as deformity of the subcutaneous patch electrode, lead fracture, and electrode malposition and migration (25).

Patients require mechanical ventilation for any of three reasons: (i) airway obstruction, (ii) disorders of gas exchange, and (iii) failure of the airway's protective mechanisms. Intubation can be performed with an oral or a nasal endotracheal tube (ETT), cricothyroidotomy, or tracheotomy. Most ETTs are opaque or have an opaque strip demarcating the tip of the tube. When the head and neck of an adult are in the neutral position, the ETT tip should ideally be in the midtrachea, approximately 4 to 7 cm from the carina. On portable radiographs, the carina projects over T5, T6, or T7 in 95% of patients, and therefore if the carina is not visible, it should be assumed to be at the level of the T4-5 interspace (26). Flexion and extension of the neck can result in 2 cm of descent or ascent of the ETT, respectively. In other words, the “hose goes where the nose goes.” When the head and neck are flexed, the ETT should ideally be 2 to 4 cm from the carina; with extension, it should be 7 to 9 cm from the carina. Therefore, it is very important to check or know the position of the head/neck before recommending tube repositioning. The inflated ETT cuff (balloon) should fill but not bulge the lateral tracheal walls (Fig. 5-24).

The most frequent complications of ETT placement include difficulty in sealing the airway, self-extubation, right main bronchus intubation, esophageal intubation, and aspiration of gastric contents (27) (Table 5-4). With right main bronchial intubation, the left lung usually collapses (Figs. 5-25 and 5-26). If the ETT is placed in the pharynx or is dislodged from the trachea, mechanical ventilation is disrupted, the stomach may distend with air, and gastric contents may be aspirated. An ETT tip placed just beyond the vocal cords may cause vocal cord injury when the cuff is inflated. Inadvertent placement of the ETT into the esophagus can be life threatening. When this occurs, the ETT may be visualized lateral to the tracheal air shadow on chest radiography, the lungs appear hypoventilated, and the stomach appears markedly distended with air. A rare complication of ETT placement is tracheal laceration; in this case, the chest radiograph may show pneumothorax, pneumomediastinum, or both. The ETT cuff may appear overdistended, as the cuff herniates through the tracheal tear. Other causes of an overdistended cuff include inadvertent cuff hyperinflation, intraesophageal cuff location, chronic intubation,
and tracheomegaly. ETT placement increases the incidence of sinusitis owing to mucosal edema and obstruction of sinus drainage.

Tracheostomy is usually performed 1 to 3 weeks after ETT placement in patients who require long-term mechanical ventilation or tracheal suctioning. The tracheostomy tube is inserted through a stoma at the level of the third tracheal cartilage, and it should be positioned with the tip several centimeters above the carina. Unlike the ETT, motion of the head and neck has little influence on the position of the tube in relation to the carina. The cuff should not extend to the tracheal wall. Following tracheostomy, subcutaneous air in the neck and upper mediastinum is common and is usually an unimportant consequence of the surgery (28). Massive air collections are caused most often by paratracheal insertion of the tube or perforation of the trachea. Pneumothorax is usually caused by inadvertent entry into the apical pleural space during surgery but may also be the result of tracheal perforation.

The incidence of serious tracheal injuries has decreased since the introduction of high-volume, low-pressure cuffs. Mucosal irritation from the tube and bacterial colonization lead to varying degrees of mucosal injury in every patient. In a small percentage of patients, the injury progresses to ulceration, which may lead to cartilage necrosis. After extubation, mucosal edema, erythema, and superficial ulcerations usually heal spontaneously. Deep ulcerations may result in permanent laryngeal scarring, tracheal stenosis, and tracheomalacia. Symptoms caused by permanent airway compromise usually appear several weeks to many months after extubation. Following extubation, all chest radiographs should be studied for the possibility of laryngeal or tracheal narrowing.

Pulmonary injury and air leak caused by mechanical ventilation occur in 5% to 50% of patients, with a higher incidence seen in patients with acute respiratory distress syndrome (29). Barotrauma develops when the alveoli are hyperdistended and rupture. The air dissects medially along the bronchovascular connective tissue to the mediastinum. Air can decompress cephalad into the visceral compartment of the neck or follow the esophagus caudad into the retroperitoneum. Retroperitoneal gas may continue along the anterior and posterior perirenal space into the properitoneal fat, and it can track along the anterior abdominal wall and chest wall and into the scrotum in men. Air may rupture into the peritoneum. If these routes do not adequately decompress the mediastinum, air ruptures the mediastinal parietal pleura and enters the pleural space.

Pleural drainage tubes are used for evacuation of pleural fluid and air (hydrothorax and pneumothorax, respectively). Several types and sizes of tubes are used, and all should be evaluated by chest radiography for proper placement of the tip and side holes. A side hole is marked by an interruption of the radiopaque identification line; it should be medial to the inner margin of the ribs (Fig. 5-27). Placement of the tube tip in the
subcutaneous tissues, a fissure, or the lung parenchyma can be diagnosed with chest radiography or CT scanning. CT scans can also be used to identify loculated pleural collections and direct the placement of drainage tubes. Location within a fissure can be suspected when the tube reproduces the anatomy of the minor or major fissure, or when the tube takes more of a horizontal rather than a vertical course as seen on a frontal chest radiograph. Tubes within fissures may become occluded by the surrounding lung. Tubes can be inadvertently advanced into the mediastinum or through the lung parenchyma, liver, spleen, or diaphragm, resulting in bronchopleural fistula, hemorrhage, and infection (20,30). After removal of a thoracostomy tube, a residual pleural or parenchymal line from the tube track is often identified on the chest radiograph (Fig. 5-28); this should not be mistaken for the visceral pleural edge of a pneumothorax. If a large amount of pleural fluid is removed at one time (e.g., >1.5 L), rapid lung re-expansion can, rarely, result in so-called "re-expansion" pulmonary edema.

Standard nasogastric tubes are used for suctioning gastric contents as well as for tube feeding. These tubes should be placed such that the tip is within the stomach, with the side port beyond the gastroesophageal junction. The most frequent misplacements are (a) incomplete insertion and (b) tube coiling within the esophagus (Figs. 5-29, 5-30, 5-31) (31). Small-bore
feeding tubes, ideally placed within the distal stomach or proximal small bowel, may be inadvertently placed into the lungs (Figs. 5-32, 5-33, 5-34), into the pleura (Fig. 5-35), or even through the diaphragm. Administration of tube feedings into the tracheobronchial tree may result in fatal pneumonia (32,33,34). Esophageal perforation can be caused by feeding tube placement. Radiographic findings secondary to the rare event of iatrogenic esophageal perforation include pleural effusion, pneumomediastinum, extraesophageal location of the tube, mediastinal widening, and mediastinal air–fluid levels.

Several different types of esophageal measurement probes may be placed in the esophagus to measure intrathoracic pressure, temperature, and pH. The tips of pressure and temperature probes are usually placed in the distal esophagus. pH probes are usually positioned with the tip 5 cm above the lower esophageal sphincter (35).