Vascular Access Complications

The possible complications associated with vascular access include bleeding, hematomas, pseudoaneurysms, retroperitoneal bleeding, arteriovenous fistulae, venous thrombi, air emboli, and arterial dissections. A pneumothorax, hemothorax, and airway compression are additional complications associated with subclavian or internal jugular venous access. Among these vascular access complications, an arterial pseudoaneurysm, arteriovenous fistula, and retroperitoneal hematoma are most common with a reported incidence of 0.28% to 1%, 0.1% to 0.86%, and 0.2% to 0.5%, respectively. A study using a routine ultrasound assessment after a vascular access reported an even higher incidence (2.2%–2.9%) of these complications, suggesting that these risks may not always be detected by a routine physical examination. Vascular access complications can be minimized by proficiency and care during vascular access. A vessel puncture with ultrasound guidance may be recommended to prevent these complications. When heparin is administered for left-sided procedures, sheaths should be removed only after the activated clotting time (ACT) is less than around 170 seconds. Reversal of anticoagulation with protamine should be considered in most of these cases. Adequate hemostasis following sheath removal is essential and may be best accomplished by specialized nursing units. Low molecular weight (LMW) heparin, if used, should not be started for at least 4 to 6 hours following the sheath removal. Most hematomas can be managed conservatively. An arteriovenous fistula complicated with a 7 F or smaller sheath may close spontaneously within a year. Therefore smaller sheaths should be used to minimize the sequelae of this complication. However, arteriovenous fistulae usually cannot be closed by an ultrasound probe compression and often require a surgical repair. An arterial pseudoaneurysm is usually associated with a large hematoma and pain usually accompanied by a bruit on examination and diagnosed by an ultrasound assessment. In general, a pseudoaneurysm is the result of inadequate compression following a sheath removal, and most common when systemic anticoagulation has been used. Pseudoaneurysms can be managed by an ultrasound-guided manual compression of the neck of the pseudoaneurysm or thrombin injection into the extravascular space. The “neck” of the pseudoaneurysm is the narrow path of blood flow between the artery, through the arterial wall, and into the pseudoaneurysm cavity. The ultrasound probe can be pushed firmly against the patient’s skin to compress the neck of the pseudoaneurysm usually for about 20 minutes. During this time, the blood within the pseudoaneurysm clots. After the probe is removed, the pseudoaneurysm will usually remain clotted especially if anticoagulation has been stopped or reversed. The procedure may require intravenous analgesia if there is significant patient discomfort. Compression is less successful if the patient is obese, because there is more fatty tissue between the skin and the neck of the pseudoaneurysm. It is also less successful if the neck of the pseudoaneurysm is wider, because it is less likely to clot during the period of compression. Finally, it is also much less successful if the patient is taking aspirin, warfarin, or another anticoagulants because these agents prevent clotting of the blood within the pseudoaneurysm. Advantages of ultrasound guided compression are that this is the least invasive method of stopping arterial blood flow into a pseudoaneurysm. If this least invasive method is not successful, a covered arterial stent placement or surgical repair should be considered. Retroperitoneal bleeding often results in orthostatic hypotension and/or anemia caused by unknown bleeding. A definitive diagnosis of this complication is made by abdominal computed tomography (CT). Retroperitoneal bleeding can usually be managed by conservative treatment but may sometimes require an arterial embolization or surgical repair.

Pericardial Effusion and Cardiac Tamponade

A pericardial effusion, with or without a tamponade, is a well-documented complication even in the most experienced centers. Cardiac tamponade may complicate any ablation procedure, but the incidence is somewhat higher with atrial fibrillation (AF) ablation (0.8%–2.9%). This is because of the complexity of the procedure, the thin walled left atrium (LA), extensive ablation, and the high level of systemic anticoagulation. Because cardiac tamponade is potentially life threatening, prompt recognition and management is essential. In the vast majority of situations, if the complication is recognized and managed expeditiously, the outcome is excellent; however, a delay in the diagnosis and treatment can lead to catastrophic results. Thus all electrophysiologists who perform catheter ablation must be prepared to immediately diagnose and treat cardiac tamponade.

Mechanism of Cardiac Tamponade

The heart lies within the pericardium, a sac composed of two layers: the visceral pericardium formed by a single layer of cells which covers the epicardium, and the thicker fibrous parietal pericardium. The pericardial space between the two layers is normally filled with a small amount of fluid, which reduces the friction from the normal torsion during cardiac contraction and relaxation. Importantly, the normal pericardial space has a significantly lower pressure than any of the cardiac chambers. Thus any breach in the myocardial wall and visceral pericardium allows blood to leak into the lower pressure pericardial space and form an effusion. The accumulation of fluid elevates the pressure within the pericardial space and impedes ventricular filling. A small amount of pericardial fluid can cause a cardiac tamponade if the pericardium is less compliant, whereas a large amount of pericardial fluid is necessary to cause tamponade when the compliance of the pericardial space is greater.

Other factors may affect the hemodynamics including the rate and volume of pericardial fluid accumulation. The occurrence and time course of cardiac tamponade therefore will vary, with tamponade physiology occurring acutely during the procedure, particularly when the area of injury is large or when a high-pressure chamber is perforated. Alternatively, some cases of cardiac tamponade develop as a slower accumulation of fluid over time and are only recognizable several hours after the procedure.

Potential Risk of a Cardiac Perforation Relevant to the Cardiac Anatomy

Cardiac tamponade is most commonly caused by a cardiac perforation occurring during catheter manipulation. Therefore it is important to understand the potential risks of a cardiac perforation relevant to the cardiac anatomy to recognize and treat, or perhaps avoid, cardiac tamponade. With respect to standard electrophysiologic procedures, the right ventricular apex is a particularly thin area of the heart rendering it prone to perforation. When placing a catheter in the right ventricle (RV) for the purpose of an electrophysiology (EP) study, it may be preferable to position the catheter in the middle of the RV near the septum, thereby avoiding the apex. The RV outflow tract is also a relatively thin area, particularly in the free wall. Care should be taken when placing catheters in this region for mapping and ablation of outflow tract tachycardias. It may be advisable to use a 4-mm-tip, nonirrigated ablation catheter in this region rather than a larger tip or externally irrigated catheter where the risk of a steam pop during RF energy delivery is higher.

The transseptal puncture is one of the most common causes of tamponade. If the transseptal needle is inadvertently exposed in the superior vena cava or right atrium, perforation can occur. If the tip of the shaped transseptal sheath is directed anteriorly while pulling it from the superior vena cava down to the fossa ovalis, it may perforate the right atrial appendage. Once the transseptal sheath is well engaged in the fossa ovalis, the potential for peril still exists. A puncture with the needle directed too posteriorly can result in a direct perforation of the posterior LA, whereas directing the needle too anteriorly can result in injury to the base of the LA appendage or root of the aorta. The damage to the base of the LA appendage usually results in tearing of this structure and often requires prompt surgical intervention.

Manipulation of catheters within the LA can also give rise to a cardiac perforation. As the ablation technology has advanced, the sheath and catheter sizes have increased. This equipment is more rigid and less forgiving when manipulating it within the heart. If any catheter or sheath is located within the LA appendage and clockwise torque is applied, there is a risk of tearing the base of the LA appendage. Likewise, there is often an invagination in the roof of the atrium that can be subject to similar trauma with manipulation of equipment within the superior aspect of the LA ( Fig. 38.1 ).

Fluoroscopic image exhibiting a left anterior oblique projection of the left atrium with contrast injected via the transseptal sheath. Notice the invagination of the left atrium in the roof between the right superior (RSPV) and left superior pulmonary veins (LSPV) ( arrow ). Care must be taken when positioning catheters not to cause trauma at this location. CS , Coronary sinus.

RF ablation is another potential cause for a cardiac perforation. Lesions associated with overheating with the development of steam pops are often extensive and may lead to myocardial rupture. Because multiple factors influence lesion formation, no set of ablation parameters can be considered absolutely safe. Nevertheless, limiting the power to less than 30 W and avoiding higher power applications with 8-mm-tip electrodes or irrigated electrodes minimizes the risk of steam pops. Intracardiac echocardiography (ICE) may be used to recognize overheating with the development of steam bubbles during nonirrigated RF applications. However, the value of ICE monitoring during open-irrigation RF applications is more challenging because the irrigated saline may obscure steam bubble detection.

Detection of a Pericardial Effusion and Cardiac Tamponade

A pericardial effusion may be suspected to occur during the procedure if there is rapid unexpected movement of a catheter that can puncture or tear the heart or if a catheter travels to a location not felt to be endocardial. Often, however, a pericardial effusion is not suspected until it has progressed to cardiac tamponade and the patient experiences a decrease in the blood pressure. Decreases in the blood pressure are not uncommon in the EP laboratory and are most often attributable to the dosing of medications for sedation or induced arrhythmias. It is important for the electrophysiologist to maintain a dialogue with those tasked with administering sedation. In the absence of such communication, administration of drugs to support the blood pressure can lead to a delay in the diagnosis of a cardiac tamponade as the underlying etiology of hypotension. When cardiac tamponade presents later following the procedure, patients often complain of a diffuse chest discomfort and shortness of breath. The chest discomfort is often similar in character to the pericardial pain some patients feel with ablation, but it is of greater intensity. If these symptoms arise, a prompt evaluation is critical. Although in these patients the effusion collects more gradually, the end hemodynamic effect is the same. Sinus tachycardia is known to be a common clinical sign of a cardiac tamponade that gradually develops. On the other hand, sinus bradycardia may be caused by a vagal reflex if cardiac tamponade rapidly develops. The absence of tachycardia thus does not exclude cardiac tamponade. Likewise, patients with sinus node dysfunction or who are pacemaker-dependent will not manifest sinus tachycardia.

An early diagnosis is essential to a successful management of this condition and should be made, whenever possible, in the EP laboratory so that treatment can be delivered urgently. It is preferable to recognize a developing pericardial effusion before the progression to a cardiac tamponade. The symptoms of a tachycardia, tachypnea, and hypotension are findings after the tamponade physiology is present. There are a number of techniques to document a pericardial effusion and tamponade, and fortunately several are readily available in the EP laboratory. The first detectable sign of a significant pericardial effusion is the decrease in the motion of the left heart border in the left anterior oblique (LAO) projection ( Video 38.1 ). This finding is because the thin layer of pericardial fluid and the negative pericardial pressure usually present in the pericardial space draws the parietal pericardium inward with the visceral pericardium during systole, leading to the normal fluoroscopic excursion. This surface tension effect is similar to two glass slides with a layer of water between them. When fluid accumulates and the intrapericardial pressure becomes positive, the parietal pericardium is no longer pulled in the same direction as the visceral pericardium during systole. The decreased excursion followed by the absence of excursion usually precedes a decrease in the arterial blood pressure. Thus the operator should always note the motion of the left heart border before placement of intracardiac catheters and examine this periodically throughout the procedure. Routine fluoroscopic monitoring of the left heart border allows for the detection of a pericardial effusion before it progresses to tamponade physiology. We have found it best to have a baseline LAO cine image at the onset of the procedure to serve as a reference for a comparison during the procedure. If an effusion is detected by this method, then immediate ultrasound imaging and preparation for a pericardial drainage in the EP laboratory should be initiated.

ICE is another useful tool for a rapid diagnosis of a pericardial effusion. When using ICE, it is preferable to obtain views from the right atrium and ventricle to evaluate the presence of a pericardial effusion at baseline. Any significant accumulation of fluid within the pericardial space during the procedure is abnormal and should lead to the reevaluation of the patient’s hemodynamic stability.

Transthoracic echocardiography is a very valuable tool for the diagnosis and management of cardiac tamponade. Reliance on transthoracic echocardiography should not, however, lead to an unnecessary delay in the diagnosis or therapy. Because the time delay to obtain a standard echocardiogram is often unacceptable, all EP laboratories should have a portable ultrasound machine immediately available to the operator. Right ventricular diastolic collapse is diagnostic of cardiac tamponade. Earlier signs of an increased intrapericardial pressure include a plethora of the inferior vena cava and right atrial collapse.

If there still exists a question as to whether an effusion is hemodynamically significant, then right heart catheterization remains the gold standard. This is often easily accomplished as venous access is typically already present in patients undergoing electrophysiologic procedures. Elevation and equalization of the central venous, right ventricular end diastolic and pulmonary capillary wedge pressures as well as an attenuation in the Y descent of the right atrial pressure waveform are the hallmark findings of tamponade.

Specific Considerations

If a perforation is a focal lesion in a low-pressure chamber such as the superior vena cava or right atrium during the transseptal puncture, then conservative management with termination of the procedure and avoidance or reversal of systemic anticoagulation may be all that is required. However, a tear in the heart or great vessels necessitates urgent surgical repair.

Patients with prior cardiac surgery that have previously had their pericardium opened are at a greatly reduced risk for cardiac tamponade. Once the pericardium has been opened, the layers of the pericardium tend to form dense adhesions and the potential space between the visceral and parietal pericardium is eliminated. Although this decreases the risk of a cardiac tamponade, it does not eliminate the potential for a perforation.

Management of Cardiac Tamponade

A flow diagram of the management of a cardiac tamponade is shown in Fig. 38.2 . The first step in the management of a cardiac tamponade is blood pressure support with volume and, if necessary, pressors. An intravenous bolus injection of atropine may help to improve the hemodynamics by blocking increased vagal tone. The accumulation of fluid within the pericardial space depends on the pressure gradient between the pericardial space and perforated structure. Rapid elevation in the blood pressure should be avoided, especially if the source of the bleeding is from the left ventricle (LV). Maintenance of a relatively low normal blood pressure is desirable to minimize this gradient. Anticoagulation should be reversed. If the patient has been administered heparin, then this can be treated with protamine (1.5 mg per 1000 units of heparin given, maximum dose 50 mg, typically after a 1 mg test dose). Likewise, if the international normalized ratio (INR) is elevated, this can be treated with vitamin K, fresh frozen plasma, and recombinant factor VII. Currently, for those patients treated with new oral anticoagulants, a specific reversal agent (idarucizumab) is available for dabigatran, a direct thrombin inhibitor, and usually results in prompt normalization of coagulation. The factor Xa inhibitors, such as apixaban, edoxaban, and rivaroxaban, can be reversed with andexanet, although this antidote has not received U.S. Food and Drug Administration approval at this time. The patient should be typed and crossmatched for blood as well. These interventions should take place simultaneously with preparation for pericardiocentesis.

Flow diagram of the management of cardiac tamponade. FFP , Fresh frozen plasma; INR , international normalized ratio.

The subxiphoid technique described by Sosa and colleagues is a preferred method of pericardial access. A pericardiocentesis kit should be located in the procedure room so that it is immediately available. When performing an urgent pericardiocentesis in this situation, because both the pericardial space and cardiac chambers are filled with blood, aspiration of the blood does not establish the location of the needle tip. The exact location of the pericardiocentesis needle may be easily confirmed by a contrast injection into the pericardial space on fluoroscopy and/or the presence of bubbles in the pericardial effusion by echocardiography. When passing the guidewire through the needle, its location within the pericardial space must be confirmed. Typically, this is done by observing the wire travel along the left heart border in the LAO projection. A pericardial drain with multiple side holes for aspiration of fluid should be placed over the guidewire.

In certain situations, such as an obese patient, a subxiphoid pericardiocentesis may be impossible. Another option that is available is an intercostal puncture. This is easiest to accomplish if there is a clear anterior effusion, which can be located with transthoracic echocardiography. The pericardiocentesis needle is directed between the ribs for the collection of fluid under echocardiogram guidance. Similar to a thoracentesis, the needle is inserted near the superior aspect of the rib to avoid damage to the intercostal nerve, artery, and vein, which travel along the inferior margin of the rib. If this condition does not exist and the patient is hemodynamically unstable, then transcardiac decompression may be performed. This is accomplished by deliberately perforating a cardiac chamber to gain access to the pericardial space.

Once access to the pericardial space is attained, the fluid should be evacuated. For low-volume effusions, this fluid can be discarded. If blood continues to accumulate in the pericardial space, the patient can be autotransfused. This is best done with an autologous blood recovery system, as a direct autotransfusion can result in a systemic inflammatory response that can result in disseminated intravascular coagulation. An allogenic blood transfusion may involve risks including transfusion reactions. A surgical repair will be required in the event the bleeding fails to stop.

Once fluid is evacuated from the pericardial space, the hypotension should resolve immediately. It is our practice to accurately measure the volume of blood aspirated every minute following initial evacuation of the effusion with pericardiocentesis. If the rate of bleeding does not decrease within the first 15 minutes, it is likely that a surgical repair will be required. If hypotension persists, other etiologies should be explored. Medications used to support the blood pressure can typically be discontinued. Patients may have a significant amount of chest discomfort because of inflammation and irritation of the pericardium. It is well treated with intrapericardial steroids (triamcinolone 20 mg). It may also be necessary to treat the patient with intravenous narcotics as well. The presence of pericardial pain is a useful indicator that the effusion has not recurred. If the patient is stable and bleeding seems to have stopped, the patient is monitored with a portable echocardiogram every 30 minutes for 2 hours and then every 4 hours. The pericardial drain is left in place for 12 to 24 hours after no further drainage is observed and removed if there is no sign of significant reaccumulation of the effusion.

For patients who continue to have active bleeding into the pericardial space, surgical management is required. Patients managed in this fashion, avoiding prolonged hypotension, have excellent long-term outcomes. If cardiac tamponade occurs during catheter ablation to treat AF, surgical repair can be combined with an epicardial MAZE procedure with or without exclusion of the LA appendage.

When a cardiac perforation occurs in the LV, the systemic blood pressure drops immediately, resulting in cardiogenic shock. In such a situation, percutaneous cardiopulmonary support should be deployed before a pericardiocentesis.