Complications of Catheter Ablation of Cardiac Arrhythmias

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Chapter 32 Complications of Catheter Ablation of Cardiac Arrhythmias

Reported rates of major complications following contemporary catheter ablation procedures vary by as much as five- to eightfold between various types of ablation procedures, ranging from 0.8% for supraventricular tachycardia (SVT), 3.4% for idiopathic ventricular tachycardia (VT), 5.2% for atrial fibrillation (AF), and 6.0% for VT associated with structural heart disease. Death is a rare complication of catheter ablation, occurring in 0.11% to 0.30% of patients with regular SVT, and in 0.31% of those with VT. Transseptal catheterization appears to be the cause of death in 0.2% of procedures.1

Local Vascular Complications

Complications at the catheter insertion sites are among the most common problems observed following catheter ablation procedures, estimated to occur in about 2% to 6% of procedures, and can cause significant morbidity. Local vascular complications are higher among females, older adults, obese patients, and those with preexisting peripheral vascular disease. Additionally, the risk is related to the type of procedure performed (right or left heart catheterization), the size and number of sheaths and catheters used during the procedure, as well as the associated periprocedural use of anticoagulant or antiplatelet agents.2 The rates of complications related to the site of vascular access are higher following catheter ablation of AF (1.8%) and VT in patients with structural heart disease (0.7% to 4.7%) compared with ablation of SVT (0.4%).1

Bleeding is the most common vascular complication. This can simply result in a local hematoma of little clinical significance. Vascular laceration can cause large hematomas in the groin and thigh. Acute bleeding generally can be controlled with prolonged manual compression. Groin hematomas usually resolve in 1 to 2 weeks if ongoing bleeding is stopped. Large hematomas can require blood transfusion, but surgical repair is rarely required. Arteriovenous fistulas and pseudoaneurysms need to be excluded in the setting of large or continually expanding hematomas. Retroperitoneal hematomas are often the result of arterial puncture above the inguinal ligament, allowing bleeding and hematoma to extend to the retroperitoneal space. Retroperitoneal hematomas should be suspected in the setting of a marked drop in hematocrit or unexplained hypotension or flank pain. Abdominal computed tomography (CT) scanning or ultrasound is required to confirm the diagnosis. Retroperitoneal bleeds are generally managed conservatively (bed rest, blood transfusion). Catheter or surgical interventions, however, can occasionally be required.3

Femoral artery pseudoaneurysms form when a tear through all the layers of the artery at the puncture site fails to seal, allowing persistent blood flow outside the vessel into a space contained by the surrounding tissue. This is in contrast to a hematoma, which has clotted blood outside the vessel with absence of flow. Pseudoaneurysms lack a fibrous wall and are contained by a surrounding shell of hematoma and the overlying soft tissues. Risk factors for pseudoaneurysm development include the use of large vascular sheaths, potent post-procedure anticoagulation, inadequacy of initial effort at hemostasis after removal of sheaths, and punctures of the femoral artery that are too distal, that is, at the level of bifurcation of the femoral artery or below. Also, multiple attempts at vascular access (arterial or venous) with inadvertent arterial puncture appear to increase the risk for pseudoaneurysm formation. Repeated damage to the arterial wall may result in weakening that leads to pseudoaneurysm development.

A pseudoaneurysm typically manifests a painful pulsatile mass with a systolic bruit or thrill, and the diagnosis is confirmed by duplex ultrasonography. Pseudoaneurysms can be complicated by rupture or distal embolization. Pseudoaneurysms that are less than 2 cm in size and not enlarging may resolve without intervention, with serial imaging to confirm spontaneous resolution; those that are enlarging or are greater than 2 cm in size can treated by ultrasound-guided compression of the “neck” connecting the pseudoaneurysm with the vessel or by percutaneous thrombin injection. Occasionally, surgical repair is required, especially for large pseudoaneurysms with a wide connection to the parent artery. Once diagnosed, a pseudoaneurysm should be treated rather than allowing the opportunity for spontaneous resolution.

Femoral arteriovenous fistulas commonly result when bleeding from the arterial puncture tracks into the adjacent venous puncture. Arteriovenous fistulas are more likely to arise when arterial and venous punctures are performed on the same side or when arterial puncture is performed below the common femoral artery, where several superficial branches of the femoral vein overlie the femoral artery. Diagnosis is made on examination with the finding of a pulsatile mass with a continuous “to and fro” bruit and confirmed by ultrasound. Many of the iatrogenic arteriovenous fistulas are small and close spontaneously within 1 year, but ultrasound-guided compression or surgical repair can be necessary. Because cardiac volume overload and limb damage are highly unlikely with persistent arteriovenous fistulas, conservative management for at least 1 year is reasonable.2

Deep venous thrombosis and pulmonary embolism are rare and can result from venous injury, especially during prolonged procedures requiring multiple venous lines, or in the setting of venous compression by a large arterial hematoma. Femoral arterial thrombosis is rare and occurs more commonly in the setting of a small vessel lumen, the use of a large-diameter sheath, preexisting peripheral vascular disease, diabetes mellitus, and female gender.

Accurate vascular puncture and effective initial control of bleeding after sheath removal are the best measures to prevent local vascular complications. Early diagnosis and management of local access-site complications are important to reduce morbidity and improve outcome.

Cardiac Perforation


Prompt recognition and management of cardiac perforation are critical to prevent the development of cardiac tamponade and potentially life-threatening hemodynamic collapse. Although the presentation often is dramatic with abrupt hypotension, it can be insidious with a more gradual fall in blood pressure. The use of an arterial line that provides continuous blood pressure monitoring can help detect early hemodynamic compromise. Sinus tachycardia is common in the setting of cardiac tamponade that gradually develops. Nonetheless, the absence of tachycardia does not exclude cardiac tamponade; in fact sinus bradycardia can develop secondary to a vagal reflex in the setting of a rapidly developing cardiac tamponade. Any chest pain that persists beyond the completion of an ablation lesion, especially if associated with hypotension and diaphoresis, should alert the operator to the possible development of pericardial effusion.2,68

Assessment of the cardiac silhouette fluoroscopically can provide the first clue, especially if a similar assessment was made at baseline. Decreased excursion of the lateral heart border on fluoroscopy in the left anterior oblique (LAO) projection, indicating accumulating pericardial effusion, usually can be seen well before a drop in blood pressure and prior to progression to cardiac tamponade. Some operators obtain a baseline LAO cine image at the onset of a procedure to serve as a reference for comparison during the procedure, followed by intermittent evaluation of the same fluoroscopic projection during the procedure.2,68

Transthoracic echocardiography is the most definitive method for confirming the development of pericardial effusion. Intracardiac echocardiography (ICE), commonly used to guide transseptal puncture for LA procedures, also can facilitate the early detection of pericardial effusions before the emergence of tamponade physiology. Most of the pericardial space is not visualized from the RA imaging venue used to visualize the interatrial septum, and limited catheter rotation is usually required. Advancing the ICE catheter into the RV and rotating the transducer against the interventricular septum can readily identify pericardial effusions (Fig. 32-1).

Perforation without tamponade may occur during placement of diagnostic catheters or while accessing the LA by transseptal catheterization; detection at this time can prevent progression to tamponade but requires a high index of suspicion. Several clues should alert the operator to the possibility of cardiac perforation, including a ventricular catheter that reaches the edge of the cardiac silhouette, high pacing thresholds at sites despite normal electrograms and apparent good tissue contact on fluoroscopy, a right bundle branch block (RBBB) complex during “RV” pacing, and a catheter tip position discordant from where it should be (i.e., an RV catheter too far leftward with intended RV apical location; Fig. 32-2). With atrial septal puncture for accessing the left heart chambers, the aorta can be inadvertently entered; if only the needle enters the aorta and this is recognized before advancing the dilator and sheath, the needle can be withdrawn and the patient monitored for stability of vital signs and with echocardiography. The procedure can be continued if there is no accumulation of pericardial fluid after 15 to 30 minutes of monitoring. If the dilator and sheath have been advanced into the aortic root before the error is recognized, it is imperative that the sheath not be removed immediately, as this can result in immediate and perhaps irretrievable hemodynamic collapse due to intractable bleeding into the pericardial space.


The management of pericardial effusion is largely determined by its relative size and hemodynamic effect. Trivial pericardial effusions, if recognized early during the procedure, should be monitored continuously but do not warrant termination of the procedure. For larger effusions, the procedure should be terminated and anticoagulation, if administered, should be reversed. Protamine is used to reverse the effects of heparin, and activated factor VII, fresh frozen plasma, and vitamin K can be used in patients with therapeutic anticoagulation with warfarin. Intravenous fluids, vasopressors, and transfusion of blood products can be required, depending on the extent of the effusion and the severity of hemodynamic decompensation. Intravenous atropine can be of value in patients with increased vagal tone.3,9

If perforation without tamponade is recognized, an echocardiogram should be obtained as a baseline. If the offending catheter is a standard 5 or 6 Fr shaft, it can often be withdrawn back into the heart while monitoring the echocardiogram for accumulation of pericardial fluid. Most often, there will be no bleeding into the pericardial space and the procedure can be continued. If systemic anticoagulation is planned for left-sided catheterization, the operator must decide how important it is to continue the procedure with the risk of bleeding into the pericardium. If a larger catheter or large vascular sheath has been inadvertently placed in the pericardial space, echocardiography should be obtained along with cardiothoracic surgical consultation. In many if not most cases, the sheath may be safely withdrawn into the heart without adverse consequences, but the team must be ready to transport the patient to an operating room for repair of a hole or tear in the wall of the affected heart chamber. In some cases, especially when the patient is fully anticoagulated, it may be prudent to transport the patient to the operating room and prepare for urgent sternotomy before removing the catheter/sheath so as to be able to rapidly enter the chest if hemodynamic collapse occurs.

Although pericardiocentesis typically is required for large pericardial effusions, smaller effusions manifesting signs of cardiac tamponade, or both, and can effectively restore hemodynamic function, it carries the potential risk of cardiac chamber laceration, inadvertent puncture of the RV, pneumothorax, and infection. In a subset of patients (especially older female patients with a small to moderate amount of pericardial effusion who are not anticoagulated), a conservative approach incorporating administration of intravenous fluids and vasopressors to address the hemodynamic consequences of cardiac tamponade was found in a recent report a reasonable initial strategy and could obviate the need for emergency pericardiocentesis.2,7

Pericardiocentesis should be performed promptly when indicated, because there is usually a narrow therapeutic time window for intervention before critical hemodynamic compromise ensues. The procedure can be performed under fluoroscopic guidance (Video 22) image. Echocardiography can also be used to guide pericardiocentesis (Video 23 image). When echocardiography is not readily available, fluoroscopy is usually adequate to guide a safe procedure, and reliance on transthoracic echocardiography should not lead to unnecessary delay in diagnosis or therapy. The technique of percutaneous pericardiocentesis is discussed in Chapter 27. In most patients, an indwelling catheter is required for a short interval after initial drainage to confirm that the bleeding has stopped and that no effusion is reaccumulating. In the event of persistence or rapid reaccumulation of the effusion, exploration by thoracic surgery can be required. Up to 13.3% of LA perforations during AF ablation require surgical closure. Autotransfusion of blood removed from the pericardial space can be of value in patients with persistent bleeding, and is best done using an autologous blood recovery system, because direct autotransfusion can result in a systemic inflammatory response.3,6,9

Early pericarditis after cardiac perforation is common. In one report, 53.3% of such patients had persistent chest pain after effusion evacuation and removal of the pericardial catheter suggestive of pericardial inflammation. Nonsteroidal antiinflammatory agents are adequate in most patients. Additionally, intrapericardial steroids (triamcinolone, 20 mg) can help reduce pericardial inflammation. Subacute reaccumulation of pericardial fluid suggestive of postcardiac injury syndrome or inflammatory pericarditis can also occur, requiring repeat pericardiocentesis.3,9


Systemic thromboembolism can complicate EP procedures in the left side of the heart. The rate of thromboembolic events is 0.4% to 2.1% for AF ablation and up to 2.8% for ablation of VT originating in the left ventricle (LV).1,4,10 In patients undergoing AF ablation, history of a prior cerebrovascular event is the most potent individual risk factor for post-ablation cerebrovascular events and is associated with a ninefold increased risk of periprocedural stroke. Additionally, the incidence of periprocedural stroke increases in a step-wise fashion with an increasing CHADS2 score (congestive heart failure, hypertension, age >75 years, diabetes, and previous stroke/transient ischemic attack).10


Prevention remains the best strategy in minimizing cerebrovascular events during left heart mapping and ablation, and this may be achieved by the following: (1) preprocedural transthoracic or transesophageal echocardiography (TEE) in patients with AF as well as those with ischemic VT with LV dysfunction; (2) aggressive intraprocedural anticoagulation, including early heparin administration (once vascular access is obtained), followed by continuous infusion to maintain the activated clotting time at greater than 300 seconds; (3) meticulous attention to sheath management, including constant infusion of heparinized saline and air filters; (4) minimizing char formation during lesion creation by regulating power delivery to prevent abrupt impedance rise; and (5) using ICE during AF ablation for early detection of intracardiac thrombi and accelerated bubble formation consistent with endocardial tissue disruption with RF application. Open-irrigation RF ablation or cryoablation, compared with standard 4- or 8-mm solid tip or closed irrigation electrodes, can potentially decrease the formation of char and thrombus at the tip of the ablation catheter.10 Administration of large doses of protamine on completion of the ablation procedure to reverse heparin abruptly can potentially promote thrombogenesis and warrants further evaluation to confirm its safety. Continuation of warfarin at a therapeutic level at the time of AF ablation can potentially be a better alternative to strategies that use bridging with heparin or enoxaparin, as it eliminates a period of inadequate anticoagulation immediately following the ablation procedure, a critical period for thromboembolic risk because of the inflammation and irritation inherently associated with ablation.12,13

In patients with severe disease of the aorta, using a long vascular sheath to advance the ablation catheter directly into the LV can potentially reduce the risk of aortic atheroembolism.

Air Embolism

Vascular air embolism is a potentially life-threatening event that can occur during left and right heart procedures. Because many cases of venous air embolism go unnoticed, the true incidence of this complication is unknown. Air embolism has been reported in the interventional radiology literature at an incidence of 0.13%.2,3,9


Small amounts of air embolized in the venous circulation are generally broken up in the capillary bed and absorbed from the circulation without significant sequelae. Embolization of large volumes of air (>5 mL/kg) can cause severe complications (shock or cardiac arrest). However, complications have been reported with as little as 20 mL of air. On the other hand, embolization of as little as 2 or 3 mL of air into the arterial circulation can be fatal.

Paradoxical air embolization into the arterial circulation can occur through direct passage of air into the arterial system via anomalous structures such as an atrial or ventricular septal defect, a patent foramen ovale, or pulmonary arterial-venous malformations. Direct arterial air embolism is caused by the introduction of air into the LA via the transseptal sheath as well as via long vascular sheaths occasionally used for catheter stabilization during transaortic mapping and ablation in the LV.3,9

With the patient in the supine position, large volumes of air rapidly entering the venous circulation typically lodge in the RVOT or pulmonary artery, and can cause RVOT obstruction, marked reduction of cardiac output, and potentially hemodynamic collapse. Also, air embolization can lead to serious inflammatory changes in the pulmonary vessels including direct endothelial damage and accumulation of platelets and fibrin. Air in the systemic circulation can induce ischemia by various mechanisms, such as obstruction of the blood flow, vasospasm, and thrombus formation because of platelet activation.

Clinical Presentation

Most cases of venous air embolism are subclinical and do not result in untoward outcomes, and even when symptomatic, they go unrecognized because of the nonspecific nature of clinical presentation that can mimic other cardiac, pulmonary, and neurological dysfunctions. Therefore, a high index of suspicion is necessary to establish the diagnosis.3

The outcome of venous air embolism is directly related to the amount of air and the rate at which it enters the vein. Spontaneously breathing patients can experience more serious consequences than those under controlled positive-pressure ventilation because they generate negative intrathoracic pressure during the respiratory cycle, facilitating air entrainment. Awake patients typically manifest shortness of breath, continuous coughing, chest pain, and a sense of “impending doom.” Jugular venous distention, hypotension, tachycardia, and electrocardiographic (ECG) signs of right heart strain (ST-T wave abnormalities) can be observed. Severe cases are characterized by cardiovascular collapse.3,9

Arterial air emboli can distribute to almost any organ and can have devastating clinical sequelae. Direct cerebral air embolism can be associated with altered mental status, seizures, and focal neurological signs. A common presentation of air embolism during LA mapping and ablation is acute inferior ischemia, heart block, or both (Fig. 32-3). This reflects preferential downstream migration of air emboli into the right coronary artery.


The optimal management of air embolism is prevention. Careful sheath management, including constant infusion of heparinized saline and air filters, should be observed. Although air can be introduced through the infusion line, it can also occur with suction when catheters are removed. Therefore, whenever catheters are removed, they need to be withdrawn slowly to minimize suction effects and the fluid column within the sheath should be aspirated simultaneously. The sheath should then be aspirated and irrigated to ascertain that neither air nor blood has collected in the sheath.3 Importantly, the entire volume of the sheath should be aspirated after initial deployment as well as after each time a catheter is removed and reinserted, in order to ensure that a continuous column of fluid is present in the sheath and disallowing the possibility of trapped air that could otherwise be introduced when a catheter is advanced through the sheath. Testing to ascertain the sheath’s capacity prior to insertion is a good practice.


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