The Core Curriculum: Cardiopulmonary Imaging, 1st Edition (2004)

Chapter 11. Lines, Tubes, and Devices

Intrathoracic lines, tubes, and devices are commonly placed, either temporarily or permanently, for the diagnosis, monitoring, or treatment of thoracic disease processes (Table 11.1). Although some are more mundane than others, such as central venous catheters and endotracheal tubes, others are more exotic, such as extracorporeal life support (ECLS) cannulas or left ventricular assist devices. New devices continue to be developed. As radiologists, it is important to recognize the normal position of these lines, tubes, and devices and abnormal positioning with knowledge of the complications that may subsequently arise. In some cases, the very lines, tubes, or devices placed into the thorax for patient care reasons may be the source of patient morbidity and even mortality.

More often than not, the many catheters, tubes, and indwelling monitoring devices used in patient care are initially placed in the correct position. However, this should not lull either the radiologist or clinician into complacency. Catheters may be incorrectly positioned when first placed or may move from their original position into an improper position. Most catheter misplacements are readily correctable and without consequence, whereas others are serious and require immediate intervention. Bekemeyer et al. (1) reported that 27% of lines and tubes were malpositioned on portable radiographs taken after initial placement and that the radiograph was instrumental in deciding whether or not to reposition the catheter in 20%.

Always review the location of all lines, tubes, and devices.


Percutaneous Indwelling Central Catheter

In the past few years the percutaneous intravascular central catheter (PICC) has been used with increasing frequency (2). A PICC is placed percutaneously into an antecubital, basilic, or brachial vein in much the same way a peripheral intravenous line is placed but using a longer catheter that extends into the large central veins of the thorax. It is used in lieu of a central venous line, often when longer term venous access is required, for up to 3 months. PICCs are made of silicone rubber and vary in size from 2.0 to 5.0 French in diameter. Because of their small diameter, they are of relatively low radiographic opacity and are often difficult to visualize with standard chest radiographic technique (Fig. 11.1A).


Because the PICC is usually placed blindly at the bedside, a postplacement chest radiograph is used to confirm proper position. To make the PICC line more recognizable radiographically, a right anterior oblique radiograph (or if portable left posterior oblique) to rotate the superior vena cava off the thoracic spine, performed using low kVp technique (65 to 70 kVp versus 120 kVp for standard chest radiography) as used for rib detail radiographs, is useful (Fig. 11.1B). Ideally, the catheter tip should be in the superior vena cava or the brachiocephalic veins (Fig. 11.1). Fluoroscopic guidance may also be used to ensure proper positioning. Compared with central venous lines, there is a lower complication rate. The risk of pneumothorax is avoided as the entry site is remote from the pleura. There is also a lower incidence of both thrombosis (Fig. 21.10) and infection. PICCs more frequently become displaced than conventional central venous lines because of their flexibility, requiring repositioning and additional imaging to confirm position (Fig. 11.2).

Table 11.1: Diagnostic, Monitoring, and Therapeutic Thoracic Lines, Tubes, and Devices

   Percutaneous indwelling central catheter
   Central venous catheter
   Pulmonary artery catheter
   Venovenous or venoarterial extracorporeal life support
   Intraaortic balloon pump
   Venoarterial extracorporeal life support
   Implantable cardiac defibrillator
   Left venticular assist device
   Atrial septal defect closure device
   Endotracheal tube
   Tracheostomy tube
   Intratracheal oxygen catheter
   Feeding tube
   Nasogastric or oral-gastric tubes
   Intraesophageal manometer
   Temperature probe
   pH probe
   Antireflux devices
   Gastric banding
   Chest tubes

Figure 11.1 Normal position of a percutaneous intravascular central catheter (PICC) line. A. Standard posteroanterior chest radiograph demonstrates the left upper extremity PICC with tip in the distal left brachiocephalic vein. B. Note the greater conspicuity of the same percutaneous intravascular central catheter on the right anterior oblique radiograph at low kVp technique.

Figure 11.2 Abnormal and normal right upper extremity percutaneous intravascular central catheter position in the same patient after repositioning several times. A. Extending up the right internal jugular vein (arrow). B. Extending through the superior vena cava into the right atrium (arrow). C. Correct position in the superior vena cava (arrow).

Low kVp radiographs taken in an oblique position make it easier to see the position of PICC lines.

Central Venous Catheter

Central venous access is used for both diagnosis, such as the measurement of central venous pressure and blood draws, and therapy, for the delivery of medications. Central venous catheters are placed percutaneously, usually through an internal jugular or subclavian vein. Less commonly, they are placed using a femoral approach, avoiding the risk of pneumothorax. The subclavian approach is less accepted because of concerns for increased infection and thrombosis and patient mobility. More permanent versions include the Hickman catheter (named after Dr. Hickman; silicone catheter with one, two, or three lumens), and various ports such as the Port-A-Cath (titanium port with a polyurethane catheter) (Sims-Deltec, Inc., St. Paul, MN). The Hickman catheter was developed in the late 1970s as a modification of the Broviac catheter developed by Dr. Broviac in 1973 for infusing total parenteral nutrition. The Hickman catheter is more widely used today, having a wider tube and thicker wall than the Broviac catheter. These are usually placed through a neck vein, tunneled under the skin, with an access point just below the clavicle. The end of the Hickman catheter is outside the patient, with a small Dacron cuff 1 inch before the exit site that acts as a barrier to infection and as an anchor. For the Port-A-Cath, access is gained after cleaning and anesthetizing the skin and then using a needle to puncture through both the skin and the rubber wall of the port’s reservoir (Fig. 11.3). Large double-lumen catheters, such as the Sorenson catheter, may be placed for temporary renal dialysis (Fig. 11.4).

Figure 11.3 Port-A-Cath. A. Posteroanterior and (B) lateral chest radiographs demonstrate the port reservoir in the left anterior chest wall and catheter entering the left subclavian vein with tip in the superior vena cava. Note the anterior curvature of this left-sided venous catheter on the lateral view (arrow). A right-sided venous catheter does not make this curve. C. Computed tomography demonstrates the port reservoir with rubber wall (white arrow)D. Computed tomography thick maximum intensity project demonstrates the course of the catheter in the chest wall, heading underneath the clavicle. Note that the catheter curves anteriorly in the left brachiocephalic vein as it crosses anterior to the aortic arch, corresponding to the curvature seen on the lateral chest radiograph, whereas the right-sided vein has a straight course.

When used for blood draws and medication delivery, the catheter tip should be located in a brachiocephalic vein or the superior vena cava. When used to measure central venous pressure, the ideal position is in the superior vena cava to avoid inaccurate measurements that may be obtained if the catheter tip abuts or is near valves within the brachiocephalic veins. When located too distally in the right atrium, there is an increased risk of atrial arrhythmias and rarely cardiac perforation. Portable radiographs are obtained after central venous catheter placement, both to confirm that the catheter is in good position (Fig. 11.4) and to look for the possible complication of pneumothorax. Table 11.2 lists the complications that may occur secondary to central venous catheters (3). Pneumothorax occurs in up to 5% of central venous catheter placements and is more common with the subclavian approach than the jugular approach. Because these catheters are usually placed blindly at the bedside, they can end up in almost any vein within the thorax, neck, or upper extremity. It is important to know the normal venous anatomy and common variants to correctly identify catheter position. Atypical placements include extension cephalad into a jugular vein, across the mediastinum into contralateral veins, down the axillary vein, into the azygous or internal mammary veins, a left-sided superior vena cava, or even the inferior vena cava and hepatic veins (Fig. 11.5). Inadvertent arterial puncture can be confirmed radiographically by location of the catheter over the aorta (Fig. 11.6). However, it is usually recognized clinically by the withdrawal of bright red blood or recognizing pulsatile blood flow from the catheter.

A central venous catheter tip should be in the superior vena cava or a brachiocephalic vein.

A catheter tip pointing at the wall of the superior vena cava may lead to rupture if not repositioned.

Figure 11.4 Normal position of central venous catheters. Catheter entering from right internal jugular vein with tip in the distal right brachiocephalic vein, and catheter (double lumen) entering from left subclavian vein with tip in the superior vena cava illustrates location of venous anatomy.

Other complications visible radiographically include venous perforation with mediastinal and/or neck hematoma and infusion of fluid into the mediastinum that may be confused radiographically for hematoma or hemothorax (Figs. 11.7A and 11.7B). Catheter fracture that may result in fragments embolizing into the pulmonary arterial circulation occurs in less than 1% of cases and may be first recognized by the radiologist (Fig. 11.7C and 11.17D). The fragments may be removed percutaneously by the interventional radiologists. The complications of thrombosis (Fig. 11.8) and infection are uncommon and usually without findings on chest radiographs; uncommonly, dilatation of the azygos vein may be found as a collateral pathway if there is thrombosis of the superior vena cava (4). The reasons behind injury or death secondary to central venous catheter placement reported to the Federal Food and Drug Administration (FDA) medical device reporting system revealed that 55% of cases were related to health care professionals (technique); 12% were due to device failure, 3% patient-related factors, 3% pathologic/physiologic (thrombosis or thromboembolism), and 28% unknown (3). Vascular perforation was responsible for 94% of the fatalities and 54% of injuries. Common reasons implicated for catheter fracture were excessive force during catheter placement or removal, excess syringe pressure when attempting to open an occlusion, shearing the catheter with an insertion needle, catheter puncture with a surgical needle, and failure to follow insert directions.

Table 11.2: Complications Secondary to Central Venous Catheters

Vascular laceration (hemothorax, chest wall/neck/mediastinal hematoma)
Infection (possible source of septic emboli)
Catheter fragmentation and embolization
Venous thrombosis
Venous stenosis

Figure 11.5 Malpositioned central venous catheters. A. Catheter placed in left internal jugular vein extends across the left and right brachiocephalic veins of the mediastinum and then cephalad into the right internal jugular vein (arrow). B. Catheter placed in right subclavian vein extends up the right internal jugular vein (arrow). C. Catheter placed in left internal jugular vein is positioned with tip in the left superior intercostal vein, seen radiographically as the “aortic nipple” (arrow). Posteroanterior (D) and lateral (E) radiographs demonstrate a central venous catheter in the azygos vein (arrowheads).

Figure 11.6 Arterial position of a catheter. A. Posteroanterior and (B) lateral radiographs demonstrate a catheter placed through a brachial artery extending into the left subclavian artery (above the clavicular head) and down the descending thoracic aorta(arrowheads).

Figure 11.7 Complications of central venous catheter placement. A. Neck hematoma (asterisk) after right internal jugular line placement attempt. Note the endotracheal tube tip is in the right main bronchus. B. Fatal right hemothorax after right internal jugular line placement attempt in a patient with undiagnosed idiopathic thrombocytopenic purpura. C. Posteroanterior and (D) lateral radiographs demonstrate a right subclavian catheter with tip overlaying the right clavicular head (arrow), as well as catheter fragments in both the right and left pulmonary arteries (arrowheads).

Figure 11.8 Thrombus in left internal jugular vein (arrow) in a patient with several recent central venous catheters.

Pulmonary Artery Catheter

Pulmonary artery pressure and resistance, cardiac output, and pulmonary capillary wedge pressure can be measured with a balloon-tipped flow-directed catheter, providing information on cardiac function and hemodynamic status. The pulmonary capillary wedge pressure reflects left atrial and ventricular filling pressures, and left ventricular volume. When positive end-expiratory pressure is being delivered or when left ventricular compliance is reduced, the pulmonary capillary wedge pressure may not accurately reflect left ventricular preload and yield a false impression of fluid status. Although the concept of using a balloon-assisted catheter for this purpose was published 15 years earlier, cardiologist H. J. C. Swan observed a sailboat moving quickly despite the calm weather at the beach in California, leading to the initial idea of devising a catheter attached with a parachute or sail-like device. Initial testing was made with a balloon-tipped catheter, which was easier to make than a sail-like device; due to its success, the parachute idea was abandoned. Cardiologist William Ganz was working on the thermodilution method of measuring cardiac output at the same time, which was incorporated into the catheter. Pulmonary artery catheters are therefore commonly referred to as Swan-Ganz catheters (5).

The basic design has remained unchanged for over 30 years (5). Ideally, the tip of a pulmonary arterial catheter should reside within a large pulmonary artery and should not be located peripheral to the interlobar pulmonary artery that forms each hilum (Fig. 11.9). The balloon should only be inflated during placement and pressure measurement and not left wedged in a small artery. Given the length of these catheters, it is not uncommon for catheters to become coiled in the heart (Fig. 11.10). Redundancy of the catheter in the right atrium and ventricle increases the risk of thrombus formation and thromboembolism (Fig. 11.10C). In addition to the complications listed in Table 11.2for central venous catheters, there are several complications unique to flow-directed pulmonary arterial catheters, as listed in Table 11.3. They include pulmonary artery perforation with pulmonary hemorrhage, pulmonary infarcts, and pulmonary artery pseudoaneurysms (Fig. 11.11) (6). Chronic positioning of a catheter in a small pulmonary artery branch may also result in pulmonary infarction.

The tip of a pulmonary artery catheter should not be distal to the hilum of the lung.

Pulmonary artery pseudoaneurysms occur due to either direct rupture of the artery by the inflated balloon or the catheter tip. Correct pressure in the inflated balloon is about 300 mm Hg; excess pressure while inflating the balloon may lead to rupture. After the artery is lacerated and blood extends into the alveolar spaces and airway, pulmonary hemorrhage manifests radiographically as alveolar consolidation and hemoptysis clinically. Rupture through the visceral pleura may lead to hemothorax. If the vessel is injured, leaving an incomplete vessel wall, a delayed pseudoaneurysm may be found, often seen later as a pulmonary nodule adjacent to the lung hila. Because of the high risk of pseudoaneurysms rupturing, they require treatment, usually using a percutaneous approach (Fig. 11.11, B and C). Contrast-enhanced computed tomography is usually performed for diagnosis, before catheter-guided treatment.

Pulmonary artery pseudoaneurysms secondary to catheter injury have a high risk of rupture.

Figure 11.9 Normal position of a pulmonary artery catheter placed through the right internal jugular vein, with tip in the proximal right pulmonary artery (arrowhead). Note the right chest wall port (large arrow) with tip in the superior vena cava (small arrow).

Figure 11.10 Malpositioned pulmonary artery catheters. A. Peripheral to the right hilum in the right lower lung. B. Several loops of catheter in the right atrium. C. Redundancy in the main pulmonary artery. D and E. Peripheral to the right hilum in the right lower lung with focal pulmonary hemorrhage on (D) the initial postcatheter placement radiograph, followed by (E) extensive pulmonary hemorrhage and hemothorax six hours later. F. Placed through right internal jugular vein, perforated a central intrathoracic vein and the parietal pleura with resultant hemothorax. Catheter coiled in the inferior aspect of the right pleural space.

Table 11.3: Complications Secondary to Pulmonary Artery Catheters

Redundancy or coiling in heart, pulmonary artery or across cardiac valves
Pulmonary infarction
Vascular laceration (hemothorax, chest wall/neck/mediastinal hematoma)
Infection (possible source of septic emboli)
Catheter fragmentation and embolization
Venous thrombosis and thromboembolism
Venous stenosis
Pulmonary artery laceration (hemorrhage, pseudoaneurysm)

Figure 11.11 Pulmonary artery pseudoaneurysm secondary to peripheral placement of a pulmonary artery catheter. Bright red blood in endotracheal tube immediately after inflation of the pulmonary artery balloon. A. Focal hemorrhage in the right lower lung (asterisk). B.Selective pulmonary angiogram of the right middle lobe demonstrates a 2-cm pseudoaneurysm arising from a subsegmental artery. C.Pulmonary angiogram after embolization with several 2- to 4-mm Gianturco coils demonstrates absent blood flow in the pseudoaneurysm.


Extracorporeal Life Support

ECLS is a form of bedside cardiopulmonary bypass used primarily for the treatment of neonatal respiratory distress. It is used less commonly in adults with acute, severe, and potentially reversible respiratory failure, with or without cardiac failure (7,8). Deoxygenated blood is removed from the venous system through a venous cannula, usually placed in the right internal jugular vein. The blood then undergoes extracorporeal oxygenation and can be returned either through a large vein or artery. In venovenous ECLS, blood is usually returned via the right internal jugular vein and less commonly a femoral vein. In venoarterial ECLS, blood is returned into a large artery, usually the common carotid artery, which is ligated in the process. Although venovenous ECLS is used for oxygenation, venoarterial ECLS is used when left ventricular cardiac support is also necessary.

On a chest radiograph the normal location of the venous cannula tip should be in the distal superior vena cava or right atrium (Figs. 11.12and 11.13). The arterial cannula should be at the top of the aortic arch or in the innominate artery immediately adjacent to the aortic arch (Fig. 11.12). It should be noted that some cannulas have a 1 to 2 cm nonradiopaque tip, so the actual position of the cannula tip is not where it appears to be radiographically. Because ECLS patients are anticoagulated and commonly have chest tubes secondary to barotrauma, it is not surprising that the thoracic complications associated with ECLS are usually related to bleeding, such as hemothorax.

Figure 11.12 Venoarterial extracorporeal life support in a patient with acute respiratory distress syndrome secondary to streptococcal pneumonia. The tip of the venous cannula (arrowheads) is in the right atrium (arrow) and the tip of the arterial cannula (open arrowheads) is in the distal common carotid artery (large arrow).

Figure 11.13 Venovenous extracorporeal life support. A single venous cannula is visible on the chest radiograph with tip at the junction of the superior vena cava and the right atrium (arrow). Note the normal position of the pulmonary artery catheter in the main pulmonary artery. There are two left chest tubes for the treatment of barotrauma in the form of pneumothorax.

Some ECLS cannulas have a nonradiopaque portion at the tip.


Intraaortic Balloon Pump

The intraaortic balloon pump (IABP) provides mechanical circulatory support and is able to supplement cardiac output by approximately 20% to 30%. Originally introduced in the late 1960s by Dr. Adrian Kantrowitz, it initially required minor surgery to insert (9), with later design improvements allowing percutaneous placement through the common femoral artery with fluoroscopic guidance, as performed today. It is commonly used for patients with acute cardiogenic shock, unstable angina, and myocardial infarction. The balloon inflates during diastole, increasing pressure in the ascending aorta and thereby increasing coronary perfusion. The balloon deflates in systole to reduce left ventricular afterload and myocardial oxygen requirements. Balloon inflation and deflation is linked to the electrocardiogram. Contraindications to placement include aortic valve regurgitation, aortic aneurysm, severe peripheral vascular disease, and coagulopathy.

The only radiopaque portion is the IABP tip, which should be located in the proximal descending thoracic aorta, at the inferior aspect of the aortic knob (Fig. 11.14). Occasionally, the lucency of the inflated balloon may be seen as well (Fig. 11.15). If the tip is positioned too proximal, it may extend into the aortic arch branch vessels, potentially injuring or occluding the left subclavian or left vertebral artery, with embolization and stroke (Fig. 11.15) (10). When the tip is positioned too distally in the descending thoracic aorta, the IABP loses its effectiveness (Fig. 11.16). It may also occlude the ostia of the renal and mesenteric arteries, which may be complicated by renal embolism or bowel ischemia (11). Complications secondary to IABPs are listed in Table 11.4. In a retrospective review of complications secondary to IABP in 580 patients, vascular complications occurred in 72 patients (12.4%). The most common complication was ipsilateral leg ischemia in 69 patients; ischemia resolved in 82% of patients, usually by IABP removal or thrombectomy, with vascular repair and fasciotomy required in 15 patients. Six patients with ischemia died with IABP in place, and 4 patients required amputation for ischemia, but survived. There were three fatal aortic perforations.

Figure 11.14 Normal position of an intraaortic balloon pump with metallic tip at the inferior aspect of the aortic knob (arrow). Note the radiolucency of the inflated balloon (arrowheads).

The tip of an IABP should be at the inferior aspect of the aortic knob.

Figure 11.15 Abnormal intraaortic balloon pump position, with tip in the left subclavian artery (white arrow). Note the pulmonary artery catheter in correct position in the right descending pulmonary artery (black arrow) and the endotracheal tube in correct position with tip 4 cm above the carina (arrowheads).

Figure 11.16 Abnormal position of an intraaortic balloon pump in a patient who underwent mitral valve replacement complicated by cardiogenic shock and was placed on extracorporeal life support (cannula tip in distal superior vena cava). She subsequently received a left ventricular assist device as a bridge to heart transplantation. A. Tip is in the distal descending thoracic aorta (arrow). The pulmonary artery catheter tip is in the right upper lobe artery (truncus anterior). There are two pericardial drains (arrowheads)B. Note the inflated balloon (arrowheads).

Table 11.4: Complications Secondary to Intraaortic Balloon Pumps

Positioned too high—stroke
Positioned too low–renal or mesenteric ischemia
Aortic perforation
Leg ischemia



Pacemakers are battery-operated devices used for the treatment of abnormal heart rhythms (12). They may be permanent, with the generator usually implanted in the anterior chest wall under local anesthesia with fluoroscopic guidance and the leads tunneled to the subclavian vein, through which they reach the heart. Temporary pacemakers may also be placed, in which case the generator is external to the patient (Fig. 11.17). Electrical impulses are sent through the wire or wires to the heart. Pacemakers function in demand mode, with a sensing device that turns on the pacemaker when the heartbeat is too slow and turns off the pacemaker when the heart rate is above a predetermined level.

Figure 11.17 Temporary transvenous pacemaker placed through the common femoral vein at the groin, through the inferior vena cava, right atrium across the tricuspid valve and into the right ventricle with tip in the right ventricular outflow tract (arrow). There is an adjacent pulmonary artery catheter, also placed from a femoral approach, with tip in the left pulmonary artery (arrowhead). The patient had complete heart block that later required a permanent pacemaker.

Pacemakers have considerably decreased in size with advances in technology, as small as 2 to 3 cm. The most common clinical indication for a pacemaker is symptomatic bradycardia. In the setting of atrial fibrillation, a single lead pacemaker is often placed, with tip in the right ventricle (Fig. 11.17). For sick sinus syndrome or advanced atrioventricular heart block, dual-lead systems are used, with leads placed into both the right atrium and the right ventricle (Fig. 11.18). More recently, biventricular pacing is being used for the treatment of heart failure (13). In this setting, there is a third lead for pacing the left ventricle, which is usually positioned in the coronary sinus (Fig. 11.19).

The coronary sinus is the major venous drainage for the left ventricular myocardium. It is important to recognize the normal location of the coronary sinus on chest radiographs. Unlike a lead traversing the tricuspid valve from the right atrium into the right ventricle in a horizontal or oblique cranial-to-caudal direction on a front chest radiograph, the coronary sinus lead takes a sharp upward turn over the spine and is more vertically oriented than the oblique course of a catheter in the right ventricular outflow tract that extends into the pulmonary artery. On a lateral chest radiograph, the coronary sinus lead leaves the right atrium and is directed posteriorly, before heading cephalad along the posterior heart border. Figure 11.20 illustrates the normal cardiac venous drainage. Contrast is injected into the coronary sinus under fluoroscopy during lead placement to confirm position.

Figure 11.18 Dual-chamber pacemaker as demonstrated on (A) posteroanterior and (B) lateral radiographs. Device was placed for syncope and bradycardia 14 years earlier. Generator is in the left anterior chest wall with lead tips in the right atrium (arrowheads) and right ventricle (arrows).

Figure 11.19 Biventricular pacemaker in a patient with ischemic cardiomyopathy. A. Posteroanterior and (B) lateral radiographs demonstrate a left anterior chest wall generator with three leads, one in the right atrium (arrow RA), one in the right ventricle (arrow RV), and a third in a venous tributary to the coronary sinus (arrow CS). The patient initially presented with syncope, inducible ventricular and supraventricular tachycardia, requiring slow-pathway ablations and a single-chamber defibrillator. Due to progression of heart failure with ejection fraction of 29% and New York Heart Association class III heart failure symptoms, he received a biventricular pacemaker.

Most device complications, listed in Table 11.5, are not visible radiographically. However, the chest radiograph sometimes demonstrates the reason for device failure. The most common location of a broken lead is adjacent to the head of the clavicle, likely related to the continuous motion of the shoulder girdle with downward force on the lead (Fig. 11.21). An unwinding of the lead or a crack is evidence of lead failure. Twiddler syndrome refers to a chest wall device that is “twiddled” by the patient, perhaps finding it a source of constant irritation. As the patient rotates the device, the lead may become redundant in the chest wall or wound around the device, with possible retraction of the lead from the location in which it is functional (Fig. 11.22). When leads fail, they are generally severed and left in place, because they become endothelialized within weeks to a few months after placement and are therefore not easily withdrawn. Percutaneous removal of entrenched leads is difficult and not widely practiced. The most common complication seen radiographically related to placement is a pneumothorax (Fig. 11.23).

The most common location of a broken lead is beneath the head of the clavicle.

Nonfunctional leads are usually detached in the chest wall and left in place, because they become covered with endothelium.


Implantable Cardiac Defibrillators

Like pacemakers, defibrillators have also considerably decreased in size with advances in technology, now as small as 4 cm. They were first used in humans in the 1980s (14). An implantable cardioverter defibrillator is used in patients at risk for recurrent sustained ventricular tachycardia or fibrillation and sudden cardiac death (15). Several trials have demonstrated that implantable cardiac defibrillators (ICDs) are better than drug therapy for improving overall survival in patients with severe ventricular arrhythmias (16). One of the more famous individuals to receive such a device is Dick Cheney, Vice President of the United States in 2002. In one series of 231 consecutive patients receiving ICDs, implantation was successful in all patients with a mean procedure time of 80 ± 32 minutes; after surgery, one pocket hematoma, one seroma, and one pneumothorax required treatment. Only six leads required repositioning at long-term follow-up averaging 453 ± 296 days; no pocket erosions or infections were reported.

Figure 11.20 Normal epicardial coronary venous anatomy. A. Frontal projection shows the anterior interventricular (AIV) and obtuse marginal (OMV) veins draining into the great cardiac vein (GCV). The oblique vein of Marshall (VM) drains into the coronary sinus (CS) at the venous valve of Viessens, marking the point of transition from the coronary sinus into the great cardiac vein at the mid atrioventricular groove. The posterior interventricular vein (PIV) joins the coronary sinus near the ostium to the right atrium. B. Lateral projection shows the anterior interventricular vein (AIV) and obtuse marginal vein (OMV) draining into the great cardiac vein (GCV). The posterior interventricular vein (PIV) joins the coronary sinus (CS) near the ostium to the right atrium. (From 

Cascade PN, Sneider MB, Koelling TM, et al. Radiographic appearance of biventricular pacing for the treatment of heart failure. AJR Am J Roentgenol2001;177:1443-1450

, with permission.)

Table 11.5: Complications Secondary to Pacemakers and Implantable Defibrillators

Malpositioned leads
Broken leads
Venous thrombosis
Venous stenosis
Generator migration (Twiddler syndrome)
Generator failure

Figure 11.21 Two examples of broken pacemaker leads. A. Lead broken beneath the left clavicular head (arrow)B. Lead broken(arrow) in the chest wall near the generator.

Figure 11.22 Twiddler syndrome. Single lead pacemaker with lead tip in right ventricle. A. Note the generator position and the adjacent redundant lead after initial insertion. B. Three years later the generator has migrated inferiorly and medially, and the redundant lead in the chest wall has unwound.

Figure 11.23 Pacemaker and implantable cardiac defibrillators. Pacemaker in the right chest wall with lead tip in the right ventricle(large arrow, top) and the larger implantable cardiac defibrillator in the left chest wall with lead tips in the right atrium (arrow) and right ventricle (arrowhead). Note the right pneumothorax, a complication of pacemaker placement.

Figure 11.24 Epicardial implantable cardiac defibrillator patches (arrows) that required thoracotomy to implant, with epicardial leads that extend to a device in the anterior abdominal wall, as demonstrated on (A) posteroanterior and (B) lateral radiographs.

When ventricular fibrillation is detected, the ICD delivers an electrical shock that defibrillates the heart and may restore the normal heartbeat. When ventricular tachycardia is detected, the ICD delivers either a smaller electrical shock, referred to as cardioversion, or a series of small rapid pacing impulses, referred to as antitachycardia pacing, to restore the normal heart beat. The ICD will also function as pacemaker and deliver small impulses to the heart during bradycardia until the heart rate returns to normal. Other features of these sophisticated devices include the storage of detected arrhythmic events and performing noninvasive electrophysiologic testing.

Similar to a pacemaker, the generator is placed subcutaneously in the anterior chest wall or, in the case of larger older devices that weighed approximately 290 g, the anterior abdominal wall. By comparison, the current third generation devices weigh in at only 97 g. The leads are either placed transvenously (Fig. 11.23), similar to a pacemaker, or they are positioned on the surface of the heart with the larger devices; the latter requires a thoracotomy for lead placement (Fig. 11.24). The most common complication seen radiographically related to placement is a pneumothorax (Fig. 11.23). Other complications, many not visible radiographically, are listed in Table 11.5 (17).

Implantable pacemakers and defibrillators are becoming smaller and smaller.

Left Ventricular Assist Devices

Left ventricular assist devices are used to bridge patients with end-stage heart failure until heart transplantation and less commonly for recovery after open heart surgery. Patients have been supported on the device for 1 to 2 years while awaiting transplantation. Based on the results of a recent trial, FDA approval is being sought for destination therapy, which is the implantation of a left ventricular assist device for end-stage heart failure in patients who are not eligible for heart transplantation (18,19). Left ventricular assist devices pull blood from the left ventricle into a pump that then sends the blood back into the aorta, bypassing the weakened left ventricle. The pumping of blood is accomplished by the cyclical inflation of a polyurethane sac adjacent to a blood reservoir. The pump is placed in the upper part of the abdomen, with a tube attached to the pump brought through the abdominal wall to the outside of the body and attached to the external control system.

The first implantable cardiac-assist device to gain FDA approval for commercial sale in the United States was the pneumatically driven HeartMate left ventricular assist system (LVAS) (Thoratec Corporation, Pleasanton, CA), powered by an external drive console. Subsequently, the vented electric LVAS was developed, powered by wearable batteries and carried using a shoulder strap, allowing for greater patient mobility. Both devices have implantable titanium pumps that connect to their drive source by a tube, which exits the body through the skin. The pumping chamber of the LVAS has afferent and efferent cannulas, giving it a unique radiographic appearance (Fig. 11.25). Textured surfaces of the HeartMate devices promote the formation of an adherent tissue lining derived from the patients’ own blood, thereby substantially reducing the risk of thromboembolism and stroke. This allows the LVAS to provide hemodynamic support without requiring systemic anticoagulation, as is used for ECLS. As of June 2002, over 6,000 LVASs have been implanted worldwide (19). A new smaller device, the implantable ventricular assist device, has been developed. It is much smaller than the LVAS, weighing approximately 1 pound, designed for use in small adults and children (19).

Figure 11.25 HeartMate left ventricular assist system. A. Computed tomography scout demonstrates the afferent cannula positioned in the apex of the left ventricle (small arrow). The efferent cannula is positioned in the ascending aorta (large arrow) and has a nonvisible radiolucent portion that creates a widened contour to the right side of the mediastinum. The asterisk marks the pump. B. Computed tomography image demonstrates the ascending aortic anastomosis (arrow) to the nonradiopaque portion of the efferent cannula. C. The efferent cannula (arrow) corresponds to the widened mediastinum on the frontal projection. D. Afferent cannula anastomosis to the left ventricular apex (arrow) surrounded by high attenuation suture and reinforcing material.

Coronary Artery Bypass Graft Markers

Coronary artery bypass grafting is an effective well-established surgical therapy for relieving angina in patients with symptomatic coronary artery disease and improving mortality in patients with depressed left ventricular function or disease involving the left main trunk (20,21,22). Autologous vein segments were first used to bypass proximal coronary lesions by Favaloro in 1967 at the Cleveland Clinic (20). Markers on the proximal aorta were introduced in the early 1970s to mark the location of the vein graft anastomosis on the aorta.

In a recent prospective study of 182 patients undergoing cardiac catheterization after coronary artery bypass graft surgery with saphenous vein grafts, patients who had markers required significantly less total procedure time, fluoroscopy time, and contrast use than patients without markers (23). This is significant, with 30% to 50% of patients undergoing saphenous vein grafting requiring catheterization within 5 years of surgery.

Figure 11.26 Large wire coronary artery bypass graft markers (arrows) as seen on (A) posteroanterior and (B) lateral radiographs.

The markers may either be large wire circles around the ostia of the graft (Fig. 11.26) or small washer-like markers (Fig. 11.27). The latter are preferred, because it is possible that the larger superior vena cava markers that encircle graft ostia could migrate from the aorta onto the graft itself and cause graft failure. They could impede repeat coronary artery bypass grafting because of the significant amount of surface area they take up on the aorta. There are rare patients in whom placing markers may not be desirable, such as patients with connective tissue disease in whom additional suturing to a fragile aortic wall may not be desirable (24). The use of markers during surgery remains a controversial technique that is not widely practiced.

Figure 11.27 Small washer-like coronary artery bypass graft markers (arrows) as seen on (A) posteroanterior and (B) lateral radiographs.

Atrial Septal Defect Closure Device

An atrial septal defect is a congential defect in the atrial wall (Chapter 19). Percutaneous atrial septal defect closure was first reported as early as 1976 (25). Design improvements since that time have resulted in smaller retrievable devices that can be implanted with much smaller catheters. Using a catheter inserted into the common femoral vein, the catheter is passed through the cardiac defect into the left atrium, using fluoroscopic and transesophageal echocardiographic guidance. The first portion of the device is pushed out of the catheter and opens in the left atrium. The catheter is backed up across the defect into the right atrium and the second pushed out of the catheter.

Figure 11.28 Patient foramen ovale closure with a CardioSEAL device in a 42-year-old woman with recurrent cerebrovascular incidents despite anticoagulation. A. Posteroanterior, (B) lateral, and (C) coned down lateral view demonstrate the metallic nitinol struts of the closure device in the location of the atrial septum.

Currently used nitinol devices include the CardioSEAL Septal Occlusion System (NMT Medical, Boston, MA) (Fig. 11.28) and the Amplatzer Septal Occluder (AGA Medical Corporation, Golden Valley, MN) (26). Each comes in various sizes depending on the size of the hole. The CardioSEAL is a double-sided umbrella-shaped nitinol device draped with Dacron cloth that resembles a double-sided miniature umbrella or clamshell; the latter is the name by which these are commonly referred. CardioSEAL has been approved by the FDA for selected patients with patent foramen ovale, ventricular septal defects, and fenestrated Fontan defects. The Amplatzer Septal Occluder is a double-disk device made of nitinol mesh connected by a cylindrical waist that can measure 2 to 26 mm, commonly referred to as a button device. The diameter of the waist corresponds to the size of the atrial septal defect; the left atrial disk is 14 mm larger than the waist and the right atrial disk 10 mm larger than the waist. The Amplatzer Septal Occluder is FDA approved for atrial septal defect and fenestrated Fontan defects as well as selected patients with patent foramen ovale. Other percutaneous AGA devices in clinical trials include the Amplatzer Duct Occluder for patent ductus arteriosus closure, the Amplatzer PFO Occluder, and the Amplatzer Muscular Ventricular Septal Occluder.

Percutaneous devices are rapidly becoming the method of choice for closure of atrial septal defects.


Endotracheal Tube

Endotracheal tubes are placed through the mouth, less commonly the nose, to maintain an open airway and facilitate ventilation in patients undergoing anesthesia, patients with no gag reflex requiring airway protection, or patients with impaired lung function requiring assisted ventilation. They range in diameter from 2 to 10 mm. In adults, 6 to 9 mm diameter tubes are generally used. The tube is usually secured with tape or a device specifically designed to secure endotracheal tubes to reduce the possibility of upward or downward movement. Adult endotracheal tubes have a balloon cuff, which when inflated serves to both maintain proper placement and prevent aspiration. Cuff pressure should be less than 30 mm Hg to prevent airway damage.

The normal position of an endotracheal tube is with the tip 2 to 6 cm above the carina (Fig. 11.15). A radiopaque stripe on endotracheal tubes is used to make them more visible and confirm position. In 10% to 15% of placements, the tube is malpositioned. This number reaches up to 25% for endotracheal tubes placed in the field by paramedics (27). Complications of endotracheal tube placement are listed inTable 11.6. Abnormal position within the esophageal occurs in 8% of attempted intubations in critically ill patients (Fig. 11.29) (28). When gastric distension is visible on the chest radiography, esophageal intubation should be suspected. Without radiography for confirmation, evaluating tube position at the bedside or prehospital can be very difficult in acutely ill or injured patients. Too distal a position, such as in a main bronchus, may result in ventilation of only one lung, with collapse of the contralateral lung (Fig. 11.30), and rarely spontaneous pneumothorax of the ventilated lung that is receiving the entire tidal volume of air. Main bronchus intubation is more common on the right than the left. When positioned too proximally, the tube may damage the vocal cords or even fall out of the airway (Fig. 11.31). It should be remembered that the endotracheal tube moves as much as 2 to 4 cm with flexion and extension of the neck with a fulcrum mechanism. With neck flexion, the tube may extend more distally and into a main bronchus, whereas with extension the tube moves more cephalad, potentially across the vocal cords.

The tip of the endotracheal tube should be 2 to 6 cm above the carina.

Table 11.6: Complications Secondary to Endotracheal Tubes

Positioned too high (vocal cord injury, falls out)
Positioned too low (right main bronchus intubation)
Main bronchus intubation (contralateral lung collapse, ipsilateral pneumothorax)
Esophageal intubation
Airway rupture
Airway stenosis

Figure 11.29 Esophageal intubation with esophageal rupture and pneumomediastinum. Gastric contents were refluxing up into the tube.

With neck flexion the tip of the endotracheal tube moves toward the carina. With extension it moves toward the vocal cords.

Other important positioning problems visible radiographically include chronic positioning of the endotracheal tube tip against the airway wall that may result in airway injury and rupture. If the balloon appears wider that the expected width of the trachea, tracheal rupture should be suspected. Pneumomediastinum and subcutaneous emphysema usually accompany it; however, if the balloon itself is occluding the site of rupture, these findings may be absent. Aspiration during intubation is a complication that may be visible on radiographs, with new alveolar opacities typically in the superior or basilar segments of the lower lobes (Fig. 11.32). Postintubation airway stenosis, a late complication after endotracheal tube placement, is discussed in Chapter 16 (Figs. 16.4 and 16.7).

An endotracheal tube balloon that appears wider than the trachea should raise concern for tracheal rupture.

Figure 11.30 Abnormal endotracheal tube position within the right main bronchus. A. Chest radiograph with tube tip in right main bronchus (arrow), complete collapse of the left lung with deviation of mediastinum to the left, including the esophagus delineated by a nasogastric tube. B. Computed tomography in another patient with tube tip in the right main bronchus, partial collapse of the left lung and shift of mediastinum towards the left.

Figure 11.31 Abnormal endotracheal tube with balloon inflated positioned within the pharynx. High position of an endotracheal tube may cause vocal cord injury.

Figure 11.32 Aspiration secondary to endotracheal intubation. A. Normal radiograph preintubation. B. Postintubation with new bibasilar alveolar opacities. Correct positioning of endotracheal tube, pulmonary artery catheter, and central venous line.

Tracheostomy Tube

A tracheostomy is placed during a surgical procedure to create a direct opening into the trachea. Although such procedures may have been documented on Egyptian tablets dating to 3600 BC, the first successful recorded tracheostomy was performed by Prasovala in the fifteenth century. Lorenz Heister coined the term “tracheostomy” in 1718. Clinical indications for a tracheostomy tube include airway obstruction at or above the level of the larynx, mechanical ventilatory support for chronic respiratory failure, and less commonly for sleep apnea. The tubes may be made of metal, plastic, or silicone; the latter two are popular because they are lightweight and there is less crusting of secretions than with a metal tube. The tubes may be cuffed, like endotracheal tubes, or uncuffed. They may also be fenestrated with an opening to permit speech through the upper airway when the external opening is blocked. There are single and double cannula tubes. Double-cannula tubes have an inner cannula that acts as a removable liner for the more permanent outer tube and can be withdrawn for brief periods to be cleaned. A tracheal button can be placed in a mature tracheostomy tract to maintain the opening; the button itself does not extend into the airway lumen. This is used mostly for sleep apnea treatment and is kept closed during the day and opened when sleeping (29,30).

Table 11.7: Complications Secondary to Tracheostomy Tubes

Positioned in soft tissues adjacent to airway
Airway stenosis
Trachea-innominate artery fistula

Figure 11.33 Tracheostomy tube positioning. A and B. Correct position. C. Incorrect position beside the airway lumen.

Table 11.7 lists the complications that may occur with a tracheostomy. Complications visible radiographically are usually related to tube position. When evaluating airway tubes it is important to confirm that they are within, and not in, the soft tissues beside the airway (Fig. 11.33). Postintubation airway stenosis is discussed in Chapter 16 (Figs. 16.4 and 16.7). Rarely, trachea-innominate artery fistula may occur, with an incidence rate of 0.6% to 0.7%, clinically manifesting as bright red arterial blood in the airway (31). It is more commonly associated with the balloon cuff and not the tip of the tube. This complication requires emergency airway control, immediate arterial compression to control the bleeding, and immediate surgical exploration to control and repair the damaged innominate artery. Radiographically, aspirated blood in the airway appears as new alveolar opacities.

Transtracheal Oxygen Catheter

Direct transtracheal oxygen therapy is used as a more efficient alternative to nasal oxygen delivery in patients requiring long-term oxygen therapy, associated with less discomfort, improved compliance and quality of life, and less morbidity. Patients describe less inconvenience and reduced social stigma usually associated with long-term oxygen therapy and less nasal crusting or obstruction, dry throat, hoarseness, cutaneous allergic reaction, and epistaxis compared with nasal cannula oxygen delivery. Direct transtracheal oxygen therapy can be administered out of the hospital using a much smaller tube than the usual endotracheal tube or tracheostomy (32,33). A polyurethane intratracheal catheter is placed transcutaneously through the anterior aspect of the neck, such as the Heimlich Micro-Trach (Ballard Medical Products Co., Midvale, UT) or the SCOOP model (Transtracheal Systems, Denver, CO), with the device connected to oxygen at the neck (Fig. 11.34). The tip should be 1 to 2 cm above the carina (34). One device, the intratracheal oxygen catheter, is tunneled from the anterior abdominal wall under the skin of the chest wall, with the connector to the tubing leading to the oxygen tank located outside the abdominal wall. These catheters measure 7 to 11 French.

Figure 11.34 Transtracheal oxygen catheter, (SCOOP type) demonstrated on coned down (A) posteroanterior and (B) lateral radiographs.


Feeding Tubes, Nasogastric and Orogastric Tubes

Esophageal tubes are commonly placed to maintain patient nutrition or to decompress the stomach. Feeding tubes are usually positioned in the stomach or duodenum (Fig. 11.35). The duodenum is preferred to minimize gastroesophageal reflux. The most common error in placement is being incorrectly positioned within the gastrointestinal system and may occur anywhere from the pharynx to the jejunum (Figs 11.36A and 11.36B). In the case of suction catheters, it is important that the side port, and not just the tube tip, is located in the stomach.

The position of feeding tubes should be confirmed radiographically before use.

Complications that may occur with esophageal tubes are listed in Table 11.8 (35). The most serious complication is inadvertent placement into the lung, which may be complicated by pneumothorax, hemorrhage, or the infusion of feeding solution into the tracheobronchial tree and/or pleural space (Fig. 11.36C and 11.36D). Inadvertent passage of the feeding tube into the tracheobronchial tree may be unrecognized if the cough reflex is depressed due to neurologic impairment or sedation. After feeding tube placements, a portable radiograph centered at the diaphragm to include both the lower thorax and upper abdomen should be obtained to confirm correct location before the tube is used. Feeding tubes are much more flexible than nasogastric and orogastric tubes and are therefore more commonly malpositioned. Rarely, tubes may perforate the esophageal wall and even be found in the pleural space (Fig. 17.11).

Figure 11.35 Correct position of feeding tubes. A. At the Ligament of Treitz. B. In the descending duodenum.


Intraesophageal Manometer, Temperature Probe, and pH Probe

Several different types of esophageal measurement probes may be placed in the esophagus to measure intrathoracic pressure, temperature, and pH. An intraesophageal manometer is a tube with pressure gauges along the surface that measures intrathoracic pressure during the respiratory cycle. It is used to evaluate esophageal contractions in patients with dysphagia and propulsion disturbances, as well as during sleep studies for the diagnosis of upper airway resistance syndrome (36). As the esophagus squeezes on the tube, the pressures are recorded and printed on graph paper similar to an electrocardiogram. The manometer is visible as a thin metallic line along the course of the esophagus, with a slightly larger metallic tip (Fig. 11.37). Temperature probes are used to give a more accurate measurement of body core temperature than the more common oral, axillary, and rectal thermometers. They are used commonly during prolonged surgery and during surgery requiring hypothermic circulatory arrest. The catheter consists of a thermistor sensor attached to a flexible vinyl-covered lead contained within a 9- to 14-French catheter. The tip is usually positioned in the distal esophagus (37). An esophageal temperature probe may be combined with an esophageal stethoscope.

Figure 11.36 Incorrect position of esophageal tubes. A. Mid-esophagus. B. Excess coils of both feeding tube and nasogastric tube in the stomach. C. In the lower right lung. D. Looped across the carina and into the bronchus intermedius.

Table 11.8: Complications Secondary to Esophageal Tubes

Malpositioned within gastrointestinal tract
Positioned within airway (pneumothorax, lung laceration/hemorrhage, pleural space)
Esophageal rupture

Figure 11.37 Intraesophageal manometer placed for monitoring during a long cervical spine fixation surgery in a trauma patient with a flail chest.

pH probes were first introduced in 1974 and are used routinely to measure pH for the diagnosis of gastroesophageal reflux disease. The 2 mm catheter with an antimony probe is usually positioned with the tip 5 cm above the lower esophageal sphincter for these measurements, with recordings taken continuously for 24 hours (38). Patients are asked to perform activities that evoke symptoms and record the onset of symptoms by pressing a button on a microcomputer data logger (worn around the waist) for correlation with the pH recordings. Simultaneous placement of probes in the distal and proximal esophagus or even intragastric probes may also be used (39).


Metallic expandable stents are used in the thorax, including the central tracheobronchial tree (Fig. 16.15), aorta (Fig. 18.27), veins (Fig. 11.38), and esophagus (Fig. 11.39) for the treatment of benign and malignant narrowing. Stents may be mesh-type (Fig. 11.38) or coil-type (Fig. 11.39). Stents are either balloon expandable or self-expandable. Tracheobronchial and aortic stents are discussed in Chapters 16 and 18, respectively. Venous and esophageal stents are discussed here.

Figure 11.38 Wire-mesh stent in the superior vena cava as seen on (A) posteroanterior and (B) lateral radiographs.

Venous stents are placed to prevent or treat superior vena cava syndrome (Fig. 11.38), with a greater than 90% success rate in the treatment of superior vena cava syndrome (40). Over 90% of superior vena cava syndrome occurs secondary to malignancy, most commonly bronchogenic carcinoma, followed by lymphoma and metastatic disease. Nonmalignant causes include thrombosis or stenosis secondary to central venous catheters or pacemaker leads, radiation-related strictures, and fibrosing mediastinitis (41).

Figure 11.39 Coil-type stent in the esophagus as seen on (A) posteroanterior and (B) lateral radiographs.

Esophageal stents may be placed under endoscopy using either local or general anesthesia for the treatment of benign and malignant esophageal strictures, including caustic ingestion or reflux-induced strictures, and esophageal carcinoma (Fig. 11.39) (42). For esophageal cancer patients, stents provide palliative relief from dysphagia and aspiration, for a disease that has a very poor prognosis. Over 90% of esophageal stents are self-expanding metallic stents; plastic stents are less commonly used. Esophageal stents come in a variety of lengths (4 to 9 cm) and are usually 2 cm in diameter. Stents placed across the gastroesophageal junction may be accompanied by severe reflux and subsequent aspiration, leading to the development of the stents with an antireflux valve that are now widely available. Stent complications include perforation, malposition, migration, and food impaction. Dilation or the insertion of a longer stent may be necessary if the reflux induces a stricture. Once in place, stent migration is difficult to correct. Stent occlusion by tumor ingrowth, as well as fistula development, can be prevented by using covered stents. Chronically, pressure necrosis of the esophageal wall with erosion may result in an esophagobronchial fistula. Erosion may also occur into the aorta, heart, or a bronchial artery.

Antireflux Devices and Gastric Banding

Approved by the FDA in 1979, the silicone gel–filled Angelchik reflux prosthesis may be placed around the gastroesophageal junction for the prevention of gastroesophageal reflux, usually after reduction of a hiatal hernia (Fig. 11.40). It has an internal diameter of 3.1 cm and is secured around the gastroesophageal junction by two reinforced Teflon straps. The Angelchik prostheses are associated with frequent complications, including dysphagia in up to 75% of patients, migration, erosion, or disruption of the ring. In up to 25% of patients they are later removed, and they are not commonly used today (43,44,45). Medical therapy and surgical therapy, including the various fundoplication procedures, are more commonly used than such prostheses.

Figure 11.40 Angelchik prostheses placed 18 years earlier during hiatal hernia repair for gastroesophageal reflux and esophagitis. A.Computed tomography scout demonstrates the two Teflon reinforced straps (arrows) and (B) axial computed tomography image shows the fluid attenuation donut around the gastroesophageal junction.

Gastric banding is performed for the treatment of morbid obesity. The LAP-BAND Adjustable Gastric Banding (LAGB) System (INAMed Health, Santa Barbara, CA) is an example of a gastric banding device available in the United States, approved by the FDA in 2001. Placed laparoscopically, it consists of a band placed around the gastric fundus to create a small upper gastric pouch. The ring diameter can be adjusted and controls the amount of food that enters the remainder of the stomach (46). A reservoir located in the subxiphoid region is used for percutaneous inflation or deflation of the ring. Figure 11.41 is an example of a gastric band.

Figure 11.41 Gastric banding for morbid obesity with subsequent reduction in weight from 498 to 344 pounds over the following 18 months, as demonstrated on (A) computed tomography scout and (B) axial computed tomography image.

Chest Tubes

A chest tube or tube thoracostomy may be placed to remove fluid or air from the pleural space. Tube drainage of fluid is referred to as closed thoracostomy drainage, as opposed to a surgical or open drainage procedure. For example, after lobectomy a pleural tube is usually left in place, and after open heart surgery one or two pericardial drains are usually left in place (Fig. 11.16A). Surgically placed tubes are usually straight semistiff tubes. A variety of other tubes may be placed, including soft and pigtail varieties. For nonloculated pleural effusions, the tube is usually positioned in the caudal aspect of the pleural space, whereas for loculated collections the tube is positioned within the loculation.

Chest tubes are usually positioned in the lower portion of the thorax to drain fluid and in the upper thorax to drain air.

Complications secondary to thoracostomy tubes are listed in Table 11.9. Radiography is used to confirm correct tube position. If a thoracostomy tube appears to be in an unusual position and overlies the lower mediastinum, it may be pericardial (Fig. 11.42). Pleural tubes may be incorrectly positioned in the chest wall, lung, mediastinum, or pleural fissures. Such malpositions may result not only in tube malfunction but also damage of adjacent structures, such as lung hematoma secondary to tube puncture, requiring lobectomy (Fig. 11.43). Tubes positioned within fissures may or may not function correctly. In a trauma setting, one series reported that 58% of tubes were positioned in a fissure (47). Computed tomography is useful in the evaluation of malfunctioning or malpositioned tubes (48). Rarely, tubes may lacerate an intercostal artery or vein during placement or from chronic erosion, with subsequent hemothorax or extrapleural hematoma, or may perforate the right ventricle or the upper abdominal viscera if the tube inadvertently is placed through the diaphragm. Infection of a previously noninfected fluid collection is a complication that is usually not visible radiographically, except for failure of drainage or the development of loculation.

Table 11.9: Complications of Thoracostomy Tubes

Malposition (chest wall, mediastinum, lung, fissure)
Infection (empyema)
Vascular laceration (intercostal artery/vein)
Cardiac laceration
Abdominal viscera laceration (liver, spleen, stomach)

Chest tubes located in a fissure may or may not function correctly.

Non–image guided thoracostomy drainage may fail due to tube malposition, fluid debris and viscosity, loculation, or a thick pleural peel. In these cases, percutaneous image-guided catheter placement for fluid drainage, using either ultrasound or computed tomography guidance, is particularly helpful for accurate localization of the loculated fluid collection to be treated. Percutaneous drainage is an alternative to more invasive surgical drainage and uses smaller drains, ranging from 8 to 16 French, than closed tube thoracostomy, which are better tolerated by patients. Imaging also can determine whether there are multiple loculations, requiring multiple drains. Intracavitary fibrinolytic therapy is a useful adjunct to tube placement when fluid collections fail tube drainage alone by breaking up adhesions and debris. Percutaneous tube drainage works well for effusions up to 4 to 6 weeks; however, for older fluid collections success is considerably less, usually due to the development of a pleural peel (49). Image-guided placement has success rates of 67% to 83% (50).

Chest tubes for the treatment of pneumothorax are usually placed in the lateral chest wall between the fifth and seventh ribs, with tip extending cephalad toward the apex of the lung (Fig. 11.13). Smaller tubes are commonly used to treat pneumothorax after percutaneous lung biopsy and may be attached to a Heimlich valve. A Tru-Close vent is a self-contained system with a small diameter soft silicone catheter placed through the upper thorax below the clavicle, attached to a small box that contains a one-way valve (Fig. 22.11).

Figure 11.42 Pericardial drain (arrowheads) placed for pericardial infection secondary to adjacent large right middle lobe lung abscess.

Figure 11.43 Two chest tubes. One punctured the lung, with resulting large pulmonary hematoma. A. Chest radiograph shows a large hematoma in the right lung. B. Computed tomography demonstrates the high attenuation hematoma surrounding the intraparenchymal chest tube, and a second chest tube in the pleural space posteromedially.


1. Bekemeyer WB, Crapo RO, Calhoon S, et al. Efficacy of chest radiography in a respiratory intensive care unit: a prospective study.Chest 1985;88:691–696.

2. Andrews JC, Marx VM, Williams DM, et al. The upper arm approach for placement of peripherally inserted central catheters for protracted venous access. AJR Am J Roentgenol 1992;158:427–429.

3. Scott WL. Complications associated with central venous catheters. Chest 1988;94:1221–1224.

4. Wechsler RJ, Sprin PW, Conant EF, et al. Thrombosis and infection caused by thoracic venous catheters: pathogenesis and imaging findings. AJR Am J Roentgenol 1993;160:461–467.

5. Paunovic B, Sharma S, Miller A. Swan-Ganz catheterization.; March 19, 2003.

6. De Lima LG, Wynands JE, Bourke ME, et al. Catheter-induced pulmonary artery false aneurysm and rupture: case report and review. J Cardiothorac Vasc Anesth 1994;8:70–75.

7. Frazier OH, Rose EA, Macmanus Q, et al. Multicenter clinical evaluation of the HeartMate 1000 IP left ventricular assist device. Ann Thorac Surg 1992;53:1080–1090.

8. Anderson HL III, Delius RE, Sinard JM, et al. Early experience with adult extracorporeal membrane oxygenation in the modern era. Ann Thorac Surg 1992;53:553–563.

9. Kantrowitz A, Tjonneland S, Freed PS, et al. Initial clinical experience with intraaortic balloon pumping in cardiogenic shock. JAMA1968;203:113–118.

10. Karlson KB, Martin EC, Bregman D, et al. Superior mesenteric artery obstruction by intraaortic counterpulsation balloon simulating embolism: a case report. Cardiovasc Intervent Radiol 1981;4:236–238.

11. Barnett MG, Swartz MT, Peterson GJ, et al. Vascular complications from intraaortic balloons: risk analysis. J Vasc Surg 1994;19:81–87.

12. ACC/AHA practice guidelines for implantation of cardiac pacemakers and antiarrhythmia devices. Circulation 1998;31:1175–1209.

13. Cascade PN, Sneider MB, Koelling TM, et al. Radiographic appearance of biventricular pacing for the treatment of heart failure. AJR Am J Roentgenol 2001;177:1447–1450.

14. Mirowski M, Reid PR, Mower MM, et al. Termination of malignant ventricular arrhythmias with an implanted automatic defibrillator in human beings. N Engl J Med 1980;303:322–324.

15. Wolfe DA, Kosinski D, Grubb BP. Update on implantable cardioverter-defibrillators: new, safer devices have led to changes in indications. Postgrad Med 1998;103.

16. Multicenter Automatic Defibrillator Implantation Trial Investigators. Improved survival with an implanted defibrillator in patients with coronary disease at high risk for ventricular arrhythmia. N Engl J Med 1996;335:1933–1940.

17. Pacifico A, Wheelan K, Nasir N, et al. Long-term follow-up of cardioverter-defibrillator implanted under conscious sedation in prepectoral subfascial position. Circulation 1997;95:946–950.

18. Rose EA, Gelijns AC, Moskowitz AJ, et al. for the Randomized Evaluation of Mechanical Assistance for the Treatment of Congestive Heart Failure (REMATCH) Study Group. Long-term use of a left ventricular assist device for end-stage heart failure. N Engl J Med2001;345:1435–1443.

19. Thoratec says nearly 6,000 of its heart assist devices have now been implanted in patients worldwide. Press Release, Thoratec Corporation, Pleasanton, CA. June 20, 2002.

20. European Coronary Surgery Study Group. Long-term results prospective randomized study of coronary artery bypass surgery in stable angina pectoris. Lancet 1982;2:172–1180.

21. Principal Investigators of CASS and Their Associates. National Heart, Lung, and Blood Institute Coronary Artery Surgery Study.Circulation 1981;63:1.

22. CASS Principal Investigators and Their Associates. Coronary Artery Surgery Study (CASS): a randomized trial of coronary artery bypass surgery: survival data. Circulation 1983;68:939–950.

23. Peterson LR, McKenzie CR, Ludbrook PA, et al. Value of saphenous vein graft markers during subsequent diagnostic cardiac catheterization. Ann Thorac Surg 1999;68:2263–2266.

24. Saffitz JE, Ganote CE, Peterson CE, et al. False aneurysm of ascending aorta after aortocoronary bypass grafting. Am J Cardiol1983;52:907–912.

25. King T, Mills M. Secundum atrial septal defects: non-operative closure during cardiac catheterization. JAMA 1976;235:2305–2309.

26. Fischer G, Kramer HH, Stieh J, et al. Transcatheter closure of secundum atrial septal defects with the new self-centering Amplatzer Septal Occluder. Eur Heart J 1999;20:541–549.

27. Katz SH, Falk JL. Misplaced endotracheal tubes by paramedics in an urban emergency medical services system. Ann Emerg Med2001;37:32–37.

28. Knapp S, Kofler J, Stoiser B, et al. The assessment of four different methods to verify tracheal tube placement in the critical care setting. Anesth Analg 1999;766–770.

29. July 7, 2002.

30. Kacker A. Tracheostomy. MEDLINE plus Health Information. Updated 10/31/01 Access date July 7, 2002.

31. Siobal M, Kallet RH, Kraemer R, et al. Tracheal-innominate artery fistula caused by the endotracheal tube tip: case report and investigation of a fatal complication of prolonged intubation. Respir Care 2001;46:1012–1018.

32. Orvidas LJ, Kasperbauer JL, Staats BA, et al. Long-term clinical experience with transtracheal oxygen catheters. Mayo Clin Proc1998;73:739–744.

32a. Hyson EA, Ravin CE, Kelley MJ, et al. Intraaortic counterpulsation balloon: radiographic considerations. AJR Am J Roentgenol1977;128:915–918.

33. Kampelmacher MJ, Deenstra M, van Kesteren RG, et al. Transtracheal oxygen therapy: an effective and safe alternative to nasal oxygen administration. Eur Respir J 1997;10:828–833.

34. SCOOP® Transtracheal Oxygen Therapy Systems. July 10, 2002.

35. Amato EJ. A nursing reference: gastrointestinal tubes and drains. Part II. Esophageal tubes. Crit Care Nurse 1983; 46–48.

36. Shah JN. Esophageal manometry. MEDLINE plus Health Information. Updated 05/25/01. Access date July 10, 2002.

37. Pearson RC, McCloy RF, Cutler WC, et al. Multichannel digital recording of intraluminal temperature in the upper gastrointestinal tract of man: techniques and analyses. Clin Phys Physiol Measure 1988;9:243–248.

38. Richard B, Colletti RB, Christie DL, et al. Indications for pediatric esophageal pH monitoring: a medical position statement of the North American Society for Pediatric Gastroenterology and Nutrition. J Pediatr Gastroenterol Nutr 1995;21:253–262.

39. Bailey MA, Katz PO. Gastroesophageal reflux disease in the elderly. Clin Geriatr 2000;8. (See alsohttp://www.mmhc.comcgarticlesCG0008bailey.html.)

40. Irving JD, Dondelinger RF, Reidy JF, et al. Gianturco self-expanding stents: clinical experience in the vena cava and large veins.Cardiovasc Intervent Radiol 1992;15:328–333.

41. Yellin A, Rosen A, Reichert N, et al. Superior vena cava syndrome: the myth—the facts. Am Rev Respir Dis 1990;141:1114–1118.

42. Moores DWO, Ilves R. Treatment of esophageal obstruction with covered, self-expanding esophageal wallstents. Ann Thorac Surg1996;62:963–967.

43. Underwood RA, Weinstock LB, Soper NJ, et al. Laparoscopic removal of an Angelchik prosthesis. Surg Endosc Ultrasound Intervent Techn 1999;13:615–617.

44. Stuart RC, Dawson K, Keeling P, et al. A prospective randomized trial of Angelchik prosthesis versus Nissen fundoplication. Br J Surg1989;76:86–89.

45. Maxwell-Armstrong CA, Steele RJ, Amar SS, et al. Long-term results of the Angelchik prosthesis for gastro-oesophageal reflux. Br J Surg 1997;84:862–864.

46. O’Brien PE, Brown WA, Smith A, et al. Prospective study of a laparoscopically placed, adjustable gastric band in the treatment of morbid obesity. Br J Surg 1999;86:113–118.

47. Curtin JJ, Goodman LR, Quebbeman EJ, et al. Thoracostomy tubes after acute chest injury: relationship between location in a pleural fissure and function. AJR Am J Roentgenol 1994;163:1339–1342.

48. Gayer G, Rozenman J, Hoffmann C, et al. Computed tomography diagnosis of malpositioned chest tubes. Br J Radiol 2000;73:786–790.

49. Moulton JS. Image-guided management of complicated pleural fluid collections. Radiol Clin North Am 2000;38:345–374.

50. Moulton JS, Benkert RE, Weisiger KH, et al. Treatment of complicated pleural fluid collections with image-guided drainage and intracavitary urokinase. Chest 1995;108:1252–1259.