Cardiac Anesthesia

## **Chapter 4**

## The Field of Cardiac Electrophysiology

*Nicholas Roma, Joshua Elmer, Bruce Ferraro, Matthew Krinock and Darren Traub*

## **Abstract**

Cardiac electrophysiology is a unique and growing field that has made numerous advances in the past 15 years. Specifically, the field is advancing in terms of types of procedures as well as scope of practice. Pacemakers, implantable cardioverter-defibrillators (ICDs), and ablations have been the cornerstone of the field and continue to treat more and more conditions. This chapter will convey a birds-eye view of the types of the procedures in electrophysiology, the indications/contraindications, and the advances in the past 15 years. Additionally, local vs. general anesthesia in these procedures as well as the indication for the type of anesthesia will be discussed. The overall aim of this chapter is to present a unique viewpoint of cardiac electrophysiology as well as elaborate on the various types of anesthesia in this field.

**Keywords:** pacemaker, implanted cardioverter defibrillator, ablation, atrial fibrillation, electrophysiology

## **1. Introduction**

Over 50 years ago, the cardiac action potential was first applied to clinical medicine [1]. This action potential includes four separate phases: resting, rapid depolarization, rapid repolarization, and a plateau phase with each of these phases correlating to a different ion channel as well as a different physiologic event in the heart [2]. The field of cardiac electrophysiology addresses and treats inherent faults within the heart's action potential as well as structural causes of cardiac arrhythmias. Historically, arrhythmias were classified into three distinct categories: abnormal impulse generation, abnormal impulse conduction, simultaneous impulse generation/ conduction [3]. Although the types of arrythmias could be distinguished, all abnormal rhythm pathophysiology were found to consistently be related to an abnormal action potential. For example, in 1991 a study was performed proving that the action potential is prolonged in hypertrophied hearts signifying the relationship between the action potential and damaged tissue [4]. Furthermore in cardiomyopathy, K+ channels have been shown to be altered also prolonging the cardiac action potential [5]. Finally in long QT syndrome a link to a specific gene affecting a specific ion channel was identified affecting the action potential and thus demonstrating that arrhythmias

can occur in structurally normal hearts if there is an abnormality in the cell's ion channels [6].

The relationship between ion channel/action potential abnormality and related cardiac structure is the foundation of cardiac electrophysiology. Pharmacology, procedures, and patient care have come from this relationship. As intensive research has been performed since the original thesis of ion channels and arrythmias, advances in the field have grown at an extremely rapid rate. Pacemakers (transcutaneous and permanent), catheter-based ablations for all type of arrythmias, cardioversions, and non-invasive cardiac monitoring have become the new norm in electrophysiology. Additionally, advances in anesthesiology have allowed shorter procedure times, more efficient procedures, and less risk. This chapter will highlight some of the most important procedures, indications for these procedures, current advances, and the role anesthesiology plays in cardiac electrophysiology.

## **2. The most common procedures of cardiac electrophysiology**

#### **2.1 Catheter ablations**

In 1886, Walter Gaskell discovered specialized muscle fibers between the atria and the ventricle caused an irregular rhythm when cut—which was the first indication of an electrical system within the heart [7]. This has since become the basis of procedures such as cardiac or catheter ablations in electrophysiology. Presently, catheter ablations are used for almost every type of cardiac arrhythmia including: paroxysmal supraventricular tachycardia (SVT), atrial fibrillation, atrial flutter, and ventricular arrhythmias including frequent premature ventricular contractions and ventricular tachycardia.

## *2.1.1 Atrial fibrillation*

Atrial fibrillation is the most common cardiac arrythmia in clinical practice with 6–12 million people predicted to suffer from this condition in the United States by 2050 [8]. The condition stems from ectopic beats typically from the pulmonary veins causing the atria to rapidly contract [9]. This arrythmia can lead to a multitude of complications including adverse remodeling as well as increased stroke risk from clot formation in stagnant blood. Atrial fibrillation is divided into three types: paroxysmal (lasting less than 7 days and self-terminating), persistent (longer than 7 days), and permanent (where there is decision to make no attempt at restoration of sinus rhythm). Typically, rapidly acting anti-arrhythmic agents especially amiodarone are first-line treatment for paroxysmal atrial fibrillation to attempt conversion. Cardioversion, an electric shock sent through the heart to reset the electrical circuit, is second line if pharmaceuticals do not work. Finally, since 85–95% of patients have their atrial fibrillation stemming from pulmonary veins, ablating these specific spots can be quite successful [10]. Treatment success rate of ablations for paroxysmal atrial fibrillation is between 65 and 75% [11]. Unfortunately, persistent atrial fibrillation is much less successful with a procedure success rate of roughly 45% [12]. Regardless, ablation therapy can be an effective treatment for atrial fibrillation particularly when combined with an anti-arrhythmic agent. A short procedure over continuous medical management can be beneficial to young and healthy individuals with a new diagnosis as well as the older population to avoid an overuse of medication.

## *The Field of Cardiac Electrophysiology DOI: http://dx.doi.org/10.5772/intechopen.107932*

The goal of atrial fibrillation ablation is to ablate or burn the connection between the pulmonary veins and the left atrium, often referred to as pulmonary vein isolation (PVI). The type of anesthesia during the procedure has also shown specific benefits. General anesthesia is preferred to IV sedation for PVI as this allows for less patient movement and improved ability to electrically map cardiac tissue with improved catheter contact [13]. Utilizing general anesthesia can improve efficacy rates and provide better patient outcomes in atrial fibrillation ablations.

At the start of atrial fibrillation ablations, a Transesophageal Echocardiogram (TEE) is performed after intubation. Of note, a paralytic is not used after intubation due to observation of the diaphragm. The TEE is utilized to look for thrombus in the Left Atrium as this is a direct contraindication to the procedure. If no thrombus is present, the procedure can continue. An additional preventive measure is esophageal temperature. Esophageal temperature is utilized because of the high frequency/temperature of the catheter used to physically ablate the pathway. This catheter reaches such high temperatures that a major potential complication of an ablation is esophageal injury. Any acute change to the temperature could indicate injury has occurred. Complications in atrial fibrillation ablations include: atrial-esophageal fistula, stroke, tamponade, and pulmonary vein stenosis. These complications were found in roughly 2.9% of the cases [14].

## *2.1.2 Atrial flutter*

Atrial flutter is best known for the saw-tooth pattern seen on EKG. This saw tooth pattern represents the abnormal electrical circuit occurring in the heart and causing rapid beating of the atrium. Atrial flutter is ideal for ablation due to the typical anatomical landmarks found in the right atrium where the ectopic beats are from. Due to this, the success rate of an atrial flutter ablation is 95% [15]. Given the high success rate of catheter ablation of atrial flutter and the difficulty of medically treating this arrythmia, ablation of atrial flutter has now moved into first-line treatment. Atrial flutter ablations are very similar to atrial fibrillation ablations in terms of anesthetic considerations. TEE still occurs after intubation and no paralytic is used after initial intubation to determine diaphragm status. Additionally, an esophageal temperature catheter is placed as atrial flutter ablations have a similar risk of esophageal injury due to high temperature/frequency being used. Other complications of atrial flutter ablations are in line with atrial fibrillation ablations including stroke, tamponade, and vascular complications.

## *2.1.3 SVT*

Paroxysmal SVT is broken down into pathway mediated tachycardia, AV nodal reentrant tachycardia and focal atrial tachycardia [10]. Pathway mediated tachycardias and AV nodal re-entrant tachycardia are disorders of impulse conduction, while focal atrial tachycardia is caused by a trigger, re-entry, or abnormal automaticity [16]. Typically, patients can present with a multitude of symptoms including palpitations, shortness of breath, and decreased exercise tolerance. The pathway of treatment for these patients starts with calcium/beta blockers or class Ic/III anti-arrhythmic agents. Depending on patient preference and success of medical therapy, catheter ablation can also be performed [17]. The focus of this type of ablation is the pre-mapping which finds the specific ectopic location or abnormal pathway in the atria and/or ventricles. This site is then ablated using radiofrequency energy or cryo-therapy with

an 85–90% success rate for cessation/cure of the arrythmia [10]. SVT ablations differ in anesthetic management. These ablations do not require intubations as the goal for this procedure is to have the patient follow commands during the procedure. During the catheter placement and ablation, the patient may be sedated more, but after these instances the patient should be able to follow commands. The overall goal is to have the patient alternate between an asleep-awake-asleep cycle with the overall goal being a dissociated patient.

Arterial lines (A-lines) in EP ablations are on a case-by-case basis. If the patient has medications that require an A-line then one will be placed. One consideration that holds true is if the patient has an ejection fraction (EF) <35%, an A-line should be placed. This A-line will allow the possibility of acute intervention if needed. Additionally, for all ablations post-operative management is similar. Patients should lay supine for 4–6 hours to prevent bleeding from the catheter sites with a pressure dressing applied. After this period of time, the patient is typically discharged to the cardiac floor for further monitoring (**Table 1**).

## **2.2 Implantable devices**

## *2.2.1 Pacemakers*

The traditional pacemaker provides an external electrical stimulus by which myocytes may be depolarized, eliciting contraction of the heart muscle (**Figure 1**) [18]. Pacemakers function when the intrinsic pacing system of the heart fails to pace effectively and quickly enough to provide an adequate cardiac output for the patient. Muscle contraction takes place almost instantaneously following electrical impulse through the process of excitation-contraction coupling. The components of the traditional pacemaker include a pulse generator, housing a battery and electrical components, and leads, which project from the device housing into the myocardium to provide the site of impulse delivery [19]. These leads in the modern pacemaker also have the capacity to sense the heart's native electric activity in specific chambers to determine when the pacemaker should provide the external stimulus, and whether that external stimulus is necessary [19].

There are many indications for the use of conventional pacemakers and these indications continue to expand with new technology. Pacemaker implantation can be considered for patients with sinus node dysfunction, acquired AV nodal conduction and HIS Purkinje pathology, neurocardiogenic syncope, neuromuscular diseases impacting cardiac tissue conduction, and congestive heart failure [19]. Equipment and techniques for pacemaker implant continue to evolve and improve the safety of this procedure but like any invasive procedure there are inherent risks associated with the procedure. Implantation of the actual pacemaker is started with a small (~5 cm)


#### **Table 1.**

*Summary of anesthesiology in ablation procedures.*

*The Field of Cardiac Electrophysiology DOI: http://dx.doi.org/10.5772/intechopen.107932*

incision in the upper chest. Then a wire is thread through the vein and into the heart. This wire connects directly to the pacemaker to generate the electric signal that is required to physically pace the heart. The type of pacemaker as well as indication of the pacemaker will determine the specific chamber(s) where the wire(s) is placed. A common placement for the wire is in the right atrium and can be confirmed via chest x-ray. Prior studies have demonstrated varying complication rates for pacemaker implantation ranging from 3 to 10% [20]. The studies have shown that both patient characteristics and center volumes impact procedural complication rates. The most frequently reported major complication related to pacemaker implants are lead related re-interventions, while hematoma is the most reported minor complication. Other possible complications can include infection, cardiac perforation, pneumothorax, and lead dislodgement [20].

Within the last 10 years, leadless cardiac pacemakers have come onto the scene as a potential alternative option to traditional cardiac pacemakers [21]. These devices were designed to offer a leadless system to avoid many of the short and long-term complications that occur with transvenous pacemaker leads. A leadless device is much smaller than a traditional pacemaker in size and these devices will continue to miniaturize. The leadless device features electronics, a lithium battery, and electrodes. Uniquely from a conventional pacemaker, however, is the fact that the device housing includes both the pulse generator and the electrode which delivers that impulse to the cardiac tissue. An attachment end is used to screw in or attach via prongs into the endocardium. Different from the traditional pacemaker, the leadless model is installed via a sheath beginning in the femoral vein and extending up to the right ventricle which can be seen on chest x-ray [21].

While leadless pacemakers share some features of transvenous pacemakers, they are much more recent in their development, and are not able to be utilized for the full range of indications of transvenous pacemakers. Leadless pacemakers are rate adaptive and may modify pacing upon detecting a patient exercising. These devices have a battery life of approximately 10 years and are externally programable, a featured shared with traditional pacemaker devices. The first leadless cardiac pacemaker was a ventricular only system: it senses and acts on a ventricle, has inhibitory activity, and features a rate response function. A newer pacemaker, the Medtronic Micra AV is able to sense the atria and pace the ventricle for patients in sinus rhythm with heart block (**Figure 2**) [22]. This newer technology, which can be seen on chest x-ray, indicates the advancement of the leadless pacemaker and the capability it has (**Figure 3**) [23].

Leadless pacemakers have a growing list of indications for use as the technology further evolves. Indications include permanent atrial fibrillation with AV block,

**Figure 2.** *Micra leadless pacemaker [Metropolitan Heart and Vascular Institute].*

**Figure 3.** *Leadless pacemaker on chest X-ray (Khader et al. [23]).*

### *The Field of Cardiac Electrophysiology DOI: http://dx.doi.org/10.5772/intechopen.107932*

second- or third-degree block in patients with normal sinus rhythm, and sinus bradycardia [24]. As uses for the leadless pacemaker expand, so does understanding of the possible complications of this device. Major complications include cardiac injury, complications at the site of entry in the groin, thromboembolism, presyncope, syncope, cardiac failure, and acute myocardial infarction, among others. Classically, the most reported of these major complications are problems at the site of catheter entry as well as perforation of the myocardium, which differs from the higher rates of electrode dislodgement, site infections, and lead fractures seen in transvenous pacemakers [21, 25]. In a study on a specific model of leadless device, the micra transcatheter pacing study, complications were reported from the 12-months postimplantation of the leadless device [26]. This study involved 745 patients at 56 centers in 19 different countries and compared prospective data on the Micra leadless system with historical data on transvenous pacemakers. Overall, the leadless system had a lower risk of major complications by a difference of 48% mostly related to the reduction in system revision. Last, no major infections have been attributed to the Micra leadless device at 12 months, which is encouraging given the infection risk seen with transvenous pacemakers [26].

As with any new technology, many opportunities exist for improvement of the leadless pacemaker. For one, improving safety of the device, and in particular, the installation process, would further set the leadless pacemaker apart from its transvenous counterpart. Specifically, modifying how the device attaches into the myocardium is one such way that has been suggested to reduce perforation risk. In addition, development of improved battery lifespan or a charging system for the battery within the pacemaker will allow for a longer device usage with fewer repeat procedures [27]. Aside from improvements in safety, the uses for the leadless pacemaker may also continue to expand with time. In fact, efforts are already underway to develop an atrial leadless pacemaker in addition to dual chamber pacing, two areas which can increase the number of patients who may benefit from such a device [28].

## *2.2.2 Implantable cardioverter-defibrillator*

Conventional transvenous implantable cardioverter defibrillators (ICDs) consist of similar components to a transvenous pacemaker: a battery, a pulse generator, and leads, which ultimately provide a pathway for shock delivery to cardiac tissue [29]. To deliver a shock, charge first accumulates within the capacitor of the device before being expelled through the leads to reach the myocardium. In addition to delivering a shock in instances of ventricular arrythmia, modern ICDs feature pacing activity similarly to pacemakers. Therapies for arrhythmia delivered by ICDs come in multiple forms, with synchronized versus asynchronized shocks as well as overdrive pacing. Synchronized and asynchronous shocks work to terminate abnormal rhythms, such as ventricular fibrillation and ventricular tachycardia, through electrical cardioversion. In contrast, overdrive pacing can be utilized in ventricular tachycardia, where the ICD transiently delivers pacing at a rate above the rate of tachycardia to cease the arrythmia. These ICD devices come in single chamber and dual chamber systems, with dual chamber systems able to discriminate between atrial and ventricular arrythmias and provide pacing output to both chambers [29]. Finally, cardiac resynchronization therapy defibrillators can be used to simultaneously pace the right and left ventricle in patients with heart failure believed to be exacerbated by conduction system disease.

Indications for an ICD include use as primary and secondary prevention. Primary prevention involves placing a defibrillator to prevent cardiac arrest in patients with

known cardiac conditions that place them at increased risk for lethal ventricular arrhythmias. These conditions include but are not limited to: ischemic and nonischemic cardiomyopathy with left ventricular ejection fraction <35%, long QT syndrome, Brugada syndrome, hypertrophic cardiomyopathy and arrhythmogenic right ventricular cardiomyopathy [30]. Secondary prevention indications include those patients who have already suffered a cardiac arrest from ventricular tachycardia or ventricle fibrillation and those patients with sustained ventricular tachycardia in the setting of structural heart disease [30]. Regarding the risks of transvenous ICDs, there are many overlaps with complications seen in transvenous pacemakers. Common risks of conventional ICD devices include lead-related issues which require revision, localized and systemic infections, cardiac perforation, and hematoma at the site of implantation [20].

Similarly, to the recent rise in leadless pacemakers as a potential alternative to transvenous pacemakers, subcutaneous ICD (S-ICD) devices have been recently developed to rival or improve upon transvenous ICD (TV-ICD) systems. These S-ICD devices are implanted within the subcutaneous tissue typically on the left side allowing for shock delivery of 80 Joules through tissue adjacent to the heart as opposed to leads directly projecting into the heart chambers (**Figures 4** and **5**) [31, 32]. This difference in function results in a different profile of complications; S-ICD complications include pocket infections and device erosion [33]. Conversely, complications of transvenous ICDs are predominantly due to its lead system and include perforation of cardiac tissue, tamponade, pneumothorax, and lead repositioning [34]. Of note, S-ICD devices may be used for many of the same indications of TV-ICDs, such as primary or secondary life-threatening arrythmia prevention or certain patients with congenital or inherited cardiac conditions (including hypertrophic cardiomyopathy, Brugada syndrome, and ischemic and non-ischemic cardiomyopathies, among others) [33]. Therefore, the advent of S-ICDs expands options for patients considering ICD implantation and allows patients and clinicians to work together in determining which risks may be best tolerated in the long term.

**Figure 4.** *Subcutaneous ICD [CardioNetworks].*

**Figure 5.** *Subcutaneous ICD location [Wikipedia].*

## *2.2.3 Further anesthetic considerations for PM and ICD*

Anesthesia for pacemaker and ICD placement traditionally required general anesthesia under the direction of an anesthesiology team. Modern approaches to sedation for device placement have involved use of a lower level of sedation and in some cases occur under a proceduralist directed, nurse administered (PDNA) model. In particular, the placement of traditional transvenous pacemakers and leadless pacemakers now favors this PDNA model to achieve conscious sedation in these patients [35]. However, the role of the anesthesiology team in such a procedure is largely determined by patient characteristics impacting the risk of such a procedure. ICD placement may also favor this PDNA model, due to an increasing push toward conscious sedation in ICD placement procedures. In fact, a conscious sedation model using opiates with benzodiazepines may be more favorable when compared to general anesthesia due to shorter procedure and recovery times as well as cost to patients [36]. In cases where sedation using Propofol is to be used, the risk of hypotension and respiratory depression must be considered. In these cases as well as cases involving deep sedation during device placement, it is recommended that proceduralists consider involvement of anesthesiology [35]. Additionally, differentiating between ICD and pacemakers on chest x-ray is imperative to ensure adequate anesthesiology pre-operative prep. To distinguish a pacemaker vs. ICD on chest x-ray, Pacemakers have small leads (**Figure 6a**), where ICD's have thick coiled segments at the end of their leads (**Figure 6b**) [37].

For patients with an active ICD, special considerations are needed for any additional procedures that these patients go through. For example, a magnet is placed over a patient with an ICD before incision and then removed after the procedure is performed. This magnet turns off the ICD shock function to ensure patient safety throughout the operation. In some cases, the ICD beeps to ensure the shock function has been disabled and will beep again when the magnet is removed. In other cases, a device representative will be present in the room to ensure the device's shock has been disabled and to interrogate the device as needed. Active pacemaker patients also have

#### **Figure 6.**

*(a) Chest X-ray ensuring lead placement in pacemaker is correct, and (b) ICD segmented coils being shown (Torres-Ayala et al. [37]).*

special considerations before surgery that need to be considered. Device interrogation should be done before and after surgery if the surgery is directly affecting the device or if any complication occurs during the procedure involving the pacemaker. Additionally, similar to ICD's magnets can be used before surgery to place the pacemaker in asynchronous mode. However, before considering using a magnet for a pacemaker there are several considerations that need to be addressed including the dependency of the pacemaker for the patient, the type of surgery, and is the pacemaker obstructing the surgical field. ICD and pacemaker patients need these special considerations before procedures to ensure the success of the operation.

## **2.3 Noninvasive and invasive cardiac monitoring for arrythmias**

Before noninvasive cardiac monitoring, many arrythmias would be missed due to the arrythmia not occurring at the specific moment the EKG was being taken. Today, various monitors allow clinicians to detect many arrythmias such as atrial fibrillation, atrial flutter, tachycardia-bradycardia syndrome, junctional rhythms, and many more outside of the office or hospital. Typically, if a patient presents with palpitations, subjective irregular heart rhythm, unexplained syncope, or other cardiac manifestations with a normal EKG; a Holter monitor or ambulatory extended monitor can be utilized. A Holter monitor or ambulatory extended monitory is a wearable device that has electrodes that record EKG's. The device can be worn between 1 day to 4 weeks but in general does not provide real time data. These devices have the downside of being cumbersome to the patient as they are bulky and limit daily activity (**Figure 7**) [38].

Mobile telemetry is similar to Holter and event recorders but involves real time monitoring by a data center that can notify a patient or physician immediately of an arrhythmia. An implantable cardiac loop recorder is a small device implanted under the skin that can track rhythm, rate, and even correlation with symptoms of the patient (**Figure 8**) [39, 40]. Implantation of loop recorders do not require IV sedation. Lidocaine is typically used to numb the area before the10–15 minute procedure. Loop recorders have a battery life up to 5 years and can store data and transmit the data almost immediately to a monitoring physician [39]. A study in 2007 showed that loop recorders were superior for the diagnosis of an arrythmia over the conventional treatment method of Holter monitor (24 hours), 4-week random EKG monitoring,

and an EP study [41]. One of the primary uses for loop recorders in the modern era is detection of occult atrial fibrillation in patients with a cryptogenic stroke. Prospective studies have demonstrated that in patients with cryptogenic stroke, when a loop recorder is placed, atrial fibrillation will be discovered in up to 30% over 3 years of monitoring [42]. Loop recorders have shown a significantly higher diagnostic yield than periodic EKG monitoring or 24 and 48 hour Holter monitoring for these patient populations [43]. From a clinical standpoint, if a patient presents to the office with any cardiac manifestations pointing to a serious cardiac arrythmia that occurs rarely throughout a 12 month period, a loop recorder may be the most cost effective and efficient diagnostic tool.

## **3. Discussion**

Cardiac electrophysiology is an ever-growing field. One of the possible advancements with EP is performing the procedures without fluoroscopy. Fluoroscopy allows the proceduralist to visualize the surgical field for ablations, pacemaker/ICD implantations, etc. The main concern with fluoroscopy is the amount of radiation exposure to the EP lab team. As Low As Reasonably Achievable (ALARA) is an implemented system to reduce radiation exposure in the lab. Certain recommendations utilizing this concept are a certain distance from the table, additional lead shielding, table height, and appropriateness of fluoroscopy [44]. As these measures are actively being done in EP labs, exposure of radiation is still imminent.

Advancements to utilize other imaging in substitution of fluoroscopy could potentially be the future of the EP lab. Imaging such as intracardiac echocardiography, cardiac MRI guidance, and 3D electromapping systems have all been proposed [45]. Using these styles of imaging could produce the same result with a much less radiation exposure risk for not only the patient, but also the physician and their team. Robotic

**Figure 8.** *Loop recorder and location of the monitor [Mobitz Heart and Rhythm Center].*

surgery is also an option as this would eliminate the number of people required to be present in the room. Overall, these advancements are still far away as there needs to be a clear indication that success rate of the procedure nor the patient outcome would not falter, but a fluoroscopy-free EP lab could be the future of electrophysiology.

## **4. Conclusion**

In conclusion, cardiac electrophysiology is an ever-growing field with many advances in recent years. The field itself has an extraordinary amount of depth and conditions that can be treated. Pacemakers, ablations, and ICDs are the forefront of electrophysiology, but the field is actively expanding into cardiac monitoring. The anesthesia management of EP procedures is quite extensive. Atrial fibrillation and Atrial flutter ablations require TEE pre-procedure as well as active esophageal temperature monitoring. SVT ablations do not require intubation, but require an extensive awake-sleep-awake cycle with the overall goal being a dissociated patient to actively monitor the patient during the procedure. ICD/pacemaker anesthesiology practice favors a PDNA model, but each patient is considered on a case-by-case basis. Anesthesiology and electrophysiology work hand in hand to give the best possible care for the patient and to ensure optimal patient outcomes.

*The Field of Cardiac Electrophysiology DOI: http://dx.doi.org/10.5772/intechopen.107932*

## **Author details**

Nicholas Roma1 \*, Joshua Elmer2 , Bruce Ferraro3 , Matthew Krinock<sup>3</sup> and Darren Traub3

1 Department of Internal Medicine, St. Luke's University Health Network, Bethlehem, Pennsylvania, USA

2 Lewis Katz School of Medicine, Temple University, Philadelphia, Pennsylvania, USA

3 Department of Cardiology, St. Luke's University Health Network, Bethlehem, Pennsylvania, USA

\*Address all correspondence to: nicholas.roma@sluhn.org

© 2022 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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[28] Vatterott PJ et al. Implant, performance, and retrieval of an atrial leadless pacemaker in sheep. Heart Rhythm. 2021;**18**(2):288-296. DOI: 10.1016/J.HRTHM.2020.09.022

[29] Glikson M, Friedman P. The implantable cardioverter defibrillator. Lancet. 2001;**357**:1107-1117

[30] Sorbera CA, Cusack EJ. Indications for implantable cardioverter defibrillator therapy. Heart Disease. 2002;**4**(3):166- 170. DOI: 10.1097/00132580-200205000- 00007

[31] ICD. CardioNetworks; 2007

[32] Robystarm07. S-ICD. Wikipedia; 2020

[33] Savarimuthu S, Roy S, Obeidat M, Harky A. Subcutaneous implantable cardioverter defibrillator: Can it overtake its transvenous counterpart. Pacing and Clinical Electrophysiology. 2021;**44**(8):1413-1420. DOI: 10.1111/ PACE.14246

[34] Knops RE et al. Subcutaneous or Transvenous defibrillator therapy. New England Journal of Medicine. 2020;**383**(6):526-536. DOI: 10.1056/ NEJMOA1915932/SUPPL\_FILE/ NEJMOA1915932\_DATA-SHARING.PDF

[35] Gerstein NS, Young A, Schulman PM, Stecker EC, Jessel PM. Sedation in the electrophysiology laboratory: A multidisciplinary review. Journal of the American Heart Association. 2016;**5**(6). DOI: 10.1161/JAHA.116.003629

[36] Bollmann A, Kanuru NK, DeLurgio D, Walter PF, Burnette JC, Langberg JJ. Comparison of three different automatic defibrillator implantation approaches: Pectoral implantation using conscious sedation reduces procedure times and cost. Journal of Interventional Cardiac Electrophysiology. 1997;**1**(3):221-225. DOI: 10.1023/A:1009768806894

[37] Torres-Ayala SC, Santacana-Laffitte G, Maldonado J. Radiography of cardiac conduction devices: A pictorial review of pacemakers and implantable cardioverter defibrillators. Journal of Clinical Imaging Science. 2014;**4**(Dec):74. DOI: 10.4103/2156-7514.148269

[38] "Holter Monitor NIH," National Heart Lung and Blood Insitute. NIH; 2013

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[40] Implantable Loop Recorder. Mobitz Heart and Rhythm Center*.* Mobitz; 2022

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[42] Liao J, Khalid Z, Scallan C, Morillo C, O'Donnell M. Noninvasive cardiac monitoring for detecting paroxysmal atrial fibrillation or flutter after acute ischemic stroke: A systematic review. Stroke. 2007;**38**(11):2935-2940. DOI: 10.1161/STROKEAHA.106.478685

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[45] Purtell CS, Kipp RT, Eckhardt LL. Into a Fluoroless future: An appraisal of fluoroscopy-free techniques in clinical cardiac electrophysiology. Current Cardiology Reports. 2021;**23**(4). DOI: 10.1007/s11886-021-01461-y

## **Chapter 5**

## Extracorporeal Membrane Oxygenation: Beyond Conventional Indications

*Akram M. Zaaqoq, Mariam Gabrial and Heidi J. Dalton*

## **Abstract**

Over the last several years, the use of extracorporeal membrane oxygenation (ECMO) has exponentially increased. As the technology advanced, the rate of devastating complications has decreased somewhat, and the utility of ECMO has expanded beyond its conventional uses in cardiogenic shock and acute respiratory distress syndrome (ARDS). Currently, ECMO can be deployed in the perioperative period with high-risk surgeries where cardiac or respiratory compromise is anticipated. Moreover, it can be utilized in difficult airway patients or patients undergoing airway surgeries, thoracic surgery patients, trauma victims and many other conditions previously excluded. The aim of this review is to highlight the ECMO-patient interaction, the indications for ECMO in the non-cardiac surgery population, ECMO management and potential complications.

**Keywords:** extracorporeal membrane oxygenation, ECMO, extracorporeal life support, ECLS, trauma, peripartum

## **1. Introduction**

Fifty years ago, the first use of extracorporeal membrane oxygenation (ECMO) was for long-term respiratory support in an adult patient with post-traumatic acute lung injury [1]. Since that report, there has been an exponential increase in the use of ECMO for both circulatory and respiratory support. Due to the advances in technology, surgical techniques, and critical care medicine, ECMO has become part of standard care for many diseases in centers which can provide ECMO support. An analysis on ECMO data from 34 states enrolled in the Healthcare Cost and Utilization Project showed a significant increase in ECMO use from 2011 through 2014 [2], with an overall rate 1.34 per 100,000 patients per year. Similarly, the analysis of The Extracorporeal Life Support Organization (ELSO) international registry from 1989 to 2013 revealed an increase in ECMO use predominantly in adult patients [3].

This substantial increase and availability have expanded the utilization of ECMO beyond being a last-resort salvage intervention when other modalities are deemed insufficient. Currently, ECMO is deployed electively to mitigate the risk and ensure the safe and successful performance of high-risk procedures in at-risk patients. Elective initiation of ECMO has been associated with better outcomes than emergent rescue placement in the setting of cardiopulmonary arrest [4]. Further, by anticipating operative risks, a multidisciplinary team can decide on and prepare the most appropriate ECMO modality to provide support if needed. Venovenous (V-V) ECMO provides adequate gas exchange if the airway or the pulmonary function is compromised but cardiac function is adequate. However, venoarterial (V-A) ECMO will provide organ perfusion when both heart and lung function are inadequate. The perioperative use of ECMO requires an understanding of the basic physiology of ECMO, when to initiate the extracorporeal support, and how to manage and monitor for potential complications. This chapter will highlight common areas of ECMO management to provide the best care for those critically ill patients.

## **2. Methods**

To address our research questions, we conducted a comprehensive review of the literature by using MEDLINE and EMBASE database on July 25th, 2022. The search strategy was focused on the indications for ECMO. Keywords and MeSH term relating to these categories were used to optimize the database search. We searched with keywords and MeSH term "Extracorporeal membrane oxygenation" OR "ECMO" OR "ECLS" AND "TREATMENT INDICATION". All relevant articles were screened. We included any related work that was published in English; explicitly described the approach and specific methods; and identified issues, challenges, strengths, and limitations. The search returned 265 titles from which 240 focused on different indications for ECMO and 25 centered around ECMO management and transport (Supplementary). We thoroughly reviewed and categorized the included articles according to their format and relevant clinical themes.

## **3. Basics and physiology of extracorporeal membrane oxygenation**

## **3.1 Basics of extracorporeal membrane oxygenation**

ECMO is an Extracorporeal Life Support (ECLS) modality, where deoxygenated blood flows into a membrane lung (oxygenator- where gas exchange occurs) and returns to the patient. The presence of the membrane lung (oxygenator) and a pump, which ensures circuit flow, are required features for ECMO. Other key components are cannulas, tubing, air-gas blender, and heat exchanger. Pressure and flow sensors are also commonly integrated into the ECMO circuit. The artificial lung is a microporous hollow fiber made from polymethylpentene (PMP) [5]. The blood surrounds the fibers and flows in the opposite direction of oxygen to obtain optimal gas exchange. The difference in partial pressure between the gas phase and the venous blood allows diffusion of oxygen (O2) across the membrane into the blood and carbon dioxide (CO2) from the blood into the fiber gas. The oxygenator is connected to, or integrated with, a heat exchanger that controls the blood temperature through conduction from warm water for warming or cooling with ice or other means. The most used pump is a centrifugal device that creates suction to drain blood and propels it forward to the return site. The positive pressure generated by the centrifugal head must be higher than the pressure in the returning site from the circuit to allow forward flow. There

## *Extracorporeal Membrane Oxygenation: Beyond Conventional Indications DOI: http://dx.doi.org/10.5772/intechopen.107883*

are multiple factors determining the blood flow through the ECMO circuit: preload (patient blood volume, vascular tone and patency, and the size and the location of the drainage cannula), afterload (size and location of the reinfusion cannula, patient blood pressure/systemic vascular resistance, the length of the tube between the pump and patient), and the resistance throughout the ECMO circuit (kinking of the tubes, connections, the degree of oxygenator clot burden). Viscosity and temperature may also affect blood flow and gas exchange.

ECMO cannulas are made from polyurethane and commonly have biocompatible hydrophilic coatings, although each manufacturer may use a different coating [6]. The drainage (inflow) cannulas are multi-stage with sizes that range from 8–32F. The return (outflow) cannulas are single stage with variable sizes and lengths based on the ECMO modality, the size of the accessed vessels, and the targeted ECMO flow. In V-V ECMO dual cannulation, femoro-femoral (Vf-Vf) configuration, the return cannula size used most in adults are 23–27F and should be placed so the distal port is at the level of the vena cava / right atrium junction. In femoral-jugular (Vf-Vj) configuration, the return cannula sizes are usually 17–25F short cannulas. In peripheral V-A ECMO, the return cannula sizes range from 15–21F. It is recommended that a distal perfusion cannula is additionally inserted (usually in the superficial femoral artery) to prevent lower limb ischemia. The size of the distal perfusion cannula often ranges from 6–8F. Finally, in dual-lumen (DL) V-V ECMO configuration, cannula sizes range from 13–32F.

## **3.2 Physiology of extracorporeal membrane oxygenation**

There are two main modes for ECMO, V-V and V-A. However, hybrid modes such as V-AV can be adopted in certain clinical situations to provide extra support or to reduce risk such as differential hypoxia (North-South syndrome).

## *3.2.1 Venoarterial extracorporeal membrane oxygenation (V-A ECMO)*

In V-A ECMO, deoxygenated venous blood is drained from the patient into the ECMO circuit, passes through the pump and oxygenator for gas exchange, and oxygenated blood is then returned to the patient's arterial circulation (**Figure 1a**). Thus, V-A ECMO provides both circulatory and respiratory support until either the heart recovers, more durable options become available, transplant occurs, or the decision is made that further care is futile and ECMO is withdrawn. The flow in V-A ECMO is adjusted to maintain adequate tissue perfusion but does not totally capture all of the native cardiac output. Providing oxygenated circulatory support reduces the requirements for vasopressors and inotropes that might increase myocardial oxygen demand, inhibit myocardial recovery or result in secondary organ damage. However, as flow back into the arterial circulation on V-A ECMO results in higher afterload than a normal physiologic state, V-A ECMO can exacerbate left ventricular (LV) failure and cause left atrial (LA) hypertension with resultant pulmonary edema or pulmonary hemorrhage. Failure of the aortic valve to open also increases risk of thrombosis from static blood in the LV [7]. As a result, offloading the LV in this circumstance is required via left ventricular venting techniques, such as low dose inotrope support or more invasive unloading efforts, through intra-aortic balloon pump, Impella device, atrial septostomy or direct placement of venting cannulas via the pulmonary vein, LA, or LV.

**Figure 1.**

*Different modes and configurations of extracorporeal membrane oxygenation (ECMO). a: Venoarterial (V-A) ECMO; b: Two cannulas V-V ECMO; c: Double lumen venovenous (V-V) ECMO; and d: Veno-arteriovenous (V-AV) ECMO.*

## *3.2.2 Venovenous extracorporeal membrane oxygenation (V-V ECMO)*

In V-V ECMO, the flow is in series with the native lung and heart, hence V-V ECMO does not provide circulatory support (**Figure 1b** and **c**). It is usually utilized in patients with hypoxic and hypercapnic respiratory failure such as severe acute respiratory distress syndrome patients. By providing adequate oxygenation and ventilation, V-V ECMO reduces the injurious effect of mechanical ventilation and thus may provide the most optimal environment for lung recovery. The ECMO flow is adjusted to capture native cardiac output and maintain set gas exchange goals. Recirculation, defined as a portion of the oxygenated blood returning from the ECMO circuit being drawn back into the drainage cannula without reaching the systemic circulation, is common to some extent in all V-V support. Recirculation can be minimized by keeping return and drainage cannulas separated by 5–10 cm and is also usually less with double lumen cannulas. Recirculation is also exacerbated by anything that restricts forward flow from the right ventricle, such as pulmonary embolus or right ventricular failure. One unique configuration of V-V ECMO is the V-PA one, in which a double cannula is inserted into the pulmonary artery. This configuration has the advantage of right ventricular support, less recirculation of oxygenated blood, and single site access with subsequent easier mobility for the patient.

## *3.2.3 Hybrid configurations*

Hybrid configurations for ECMO are considered when the patient on either V-V or V-A ECMO experience certain complications that further impact the heart or the lung functions during the ECMO support (**Figure 1d**). V-A ECMO provides circulatory

## *Extracorporeal Membrane Oxygenation: Beyond Conventional Indications DOI: http://dx.doi.org/10.5772/intechopen.107883*

and respiratory support. However, it increases the left ventricular afterload, impairs ventricular drainage, and predisposes the patient to pulmonary edema. As the heart recovers, differential oxygenation happens in the upper body because of partially impaired lung function [8]. This "North-South" phenomenon necessitate consideration of hybrid configuration such as V-AV ECMO to overcome [9]. In V-V ECMO, the development of myocardial dysfunction such as right ventricular failure, might require insertion of arterial return cannula to provide the required circulatory support, for example VV-A or VV-VA ECMO configuration [10].

## *3.2.4 Targets of extracorporeal life support*

Targets for ECMO support depends on the indications for ECMO initiation, the patient clinical conditions, and the degree of underlying organ dysfunction. In V-A ECMO, the main goal is to maintain the organ-systems perfusion and to prevent organ-system failure until the heart recovers or more durable option is established. In V-A ECMO the ECMO flow determines the oxygen delivery to the tissues. Most centers aim for mixed venous oxygen saturation > 70% [11]. In addition to ECMO flow, increasing the oxygen carrying capacity can be increased by blood transfusion to higher hemoglobin goal or reducing the oxygen consumption by sedating the patient and establish invasive mechanical ventilation. On the other hand, in V-V ECMO the main goal is to establish adequate gas exchange to the tissues and allow resting settings on mechanical ventilation. Generally, tidal volume less than 4 cc/kg of IBW, plateau pressure around 25 cm H2O, and driving pressure < 14 [12].

## *3.2.5 Monitoring of extracorporeal membrane oxygenation*

Monitoring of the ECMO circuit performance is of the utmost importance because it reflects the interaction between the patient and the machine, and changes noted earlier can prevent compromise of the patient's clinical status. Upon ECMO initiation, the flow that meets the patient's clinical needs and goals for hemodynamics and gas exchange is established. This becomes continuously monitored and adjusted to meet set goals. Serial correlations between the rotations per minute (RPM) and the resultant ECMO flow is important to be aware of, and when it changes (the same RPM achieving lower ECMO flows), this could indicate hypovolemia, vasodilation, blood loss, a kink in the circuit or anything that prevents drainage of blood to the circuit or return to the body. Ideally ECMO flows in adults should target above 2 LPM to avoid circuit clotting.

Additionally, multiple points of pressure measurements across the ECMO circuit are often continuously monitored and important to be aware of. Venous pressure (P vein, also called P1 or other names dependent on manufacturer) is the pressure in the drainage line, and it is usually a negative pressure measurement as the centrifugal pump suctions blood from the body. Normal values should be set based on maintaining negative pressure values <100 cm H20 across the pressure drop of the cannula. These values are provided by pressure flow charts for every cannula via the manufacturer. An increase in the venous pressure (more negative) is indicative of hypovolemia, kinking of the drainage line or clot in the drainage cannula. Arterial pressure (P artery) is the positive pressure in the reinfusion cannula and should not exceed 300 cm H2O. An increase reflects an increase in the afterload (e.g., hypertension), kinking in the reinfusion line or a clot in the return cannula. Δ P is the pressure across the membrane lung and is measured at pre and post membrane lung sites. Values

may change based on surface area and flow but should be tracked serially and often initially are less than 20 cm H2O. The increase in Δ P across the membrane lung may indicate significant clot in the oxygenator. The ability to be aware of and understand the significance of other changes is also important as an ECMO provider, with many courses available internationally and knowledge assessments available via industry (Innovative ECMO Concepts; ECMO advantage and others) as well as organizations such as ELSO, CHEST, ATS, SCCM, and others.

#### **3.3 Extracorporeal membrane oxygenation related complications**

The complications related to ECMO support are relatively common and associated with increased morbidity and mortality. These complications can be categorized into general complications related to ECMO use, mode specific as well as disease related (**Table 1**). Bleeding is the most common complication; it occurs in almost 10–30% of patients [13]. It occurs more frequently in V-A ECMO patients than in V-V patients. In a cohort study of 158 patients, 37% of V-A ECMO patients required interventions to control the bleeding, while only 17% of the V-V ECMO ones [14]. The most common sites of bleeding are the invasive procedure sites such as the surgical incisions, cannulation sites, thoracostomy tubes, tamponade, or retroperitoneal bleeding. However, bleeding can occur anywhere, such as intracranial hemorrhage, pulmonary hemorrhage, or gastrointestinal bleeding [15]. The risk of bleeding on ECMO is related to the use of systemic anticoagulants, depletion of the coagulation factors, mainly Von Willebrand factor (vWF) by the extracorporeal circuit, platelet activation, and consumption [16]. The management of bleeding relay on stopping anticoagulants, correct coagulopathy, transfuse as needed, and surgical interventions as indicated.

Thromboembolic complications could happen but now with biocompatible devices it is less of an issue. Thrombosis could happen in the patient or the circuit. Micro thrombosis of the oxygenator is common. It is estimated 10–16% of the oxygenator develop thrombi with subsequent decrease in the ECMO efficiency [17]. Air embolism can happen if there is a break in the negative side of the circuit or with excessive drainage and subsequent air cavitation. There thrombotic event can lead to devastating neurological or systemic complications. Hence the routine use of systemic anticoagulation is adopted by most ECMO centers. A challenging scenario is heparin induced thrombocytopenia (HIT). Despite being a rare complication, it carries significant morbidity and mortality. So early recognition and utilization of direct thrombin inhibitors are advised [18].

Another common complication for patients on ECMO is secondary infection. In a retrospective cohort analysis of 145 patients on ECMO, 44.8% developed sepsis [19]. The risks for infection in patients with ECMO are related to the severity of illness, the immunocompromised status related to the underlying medical condition, the presence of invasive devices. Diagnosis of infection requires a high index of suspicion. The presence of hypo or hyperthermia, hemodynamic instability, increased oxygen requirement with desaturation, respiratory secretions, frank pyuria or worsening of renal or liver function, alteration in sensorium, coagulopathy, and new skin lesions [20]. White blood cell count might not a reliable marker for infection [21]. Other markers of inflammation like C-reactive protein (CRP) or erythrocyte sedimentation rate (ESR) could be helpful but remain non-specific. In a study of 220 V-A ECMO patients on ECMO, the most common sources of infection were ventilator-associated pneumonia (VAP) (55%), blood-stream infection (18%), cannula infections (10%), and mediastinitis (11%) [22]. Infection control should focus on prevention by



#### **Table 1.**

*Common complications during extracorporeal membrane oxygenation (ECMO) support.*

adherence to the universal hand hygiene and sterile techniques during the insertion. There is no evidence to support the use of prophylactic antibiotics in ECMO patients. For treating a suspected infection, the choice of antibiotics should be made based on the index of suspicion and the local antibiogram recommendations for each institution.

Neurological complications rates vary based on the patient characteristics, underlying medical conditions, and the mode of ECMO support. In a retrospective analysis of single-center experience, 13.3% of ECMO patients experienced neurological complications [23]. Most commonly ischemic stroke (7.0%), intracerebral hemorrhage (3.4%), hypoxic ischemic encephalopathy (3.6%), and spinal cord injury (1.2%). Neurological complications were more common in V-A ECMO (18%) rather than V-V ECMO (4.6%). ECMO especially V-A increases the risk of stroke through thromboembolism, differential oxygenation, and the associate coagulopathy. It is imperative to monitor the patient neurological examination and conduct frequent neurological assessment to recognize early neurological complications and to provide the appropriate interventions.

Vascular complications are more common in the V-A ECMO patients as well. Vascular complications are major cause of mortality. In a study, the vascular complications led to increase the mortality from 18 to 49% [24]. Acute limb ischemia affects 10–70% of the V-A ECMO patients [25, 26]. Other forms of vascular complications are dissection,

### *Extracorporeal Membrane Oxygenation: Beyond Conventional Indications DOI: http://dx.doi.org/10.5772/intechopen.107883*

pseudoaneurysm, and retroperitoneal hematomas. The risk of vascular complications is higher in women, small patients, difficult cannulation, and patients without distal perfusion cannulas. Early identification is by physical examination that shows signs of malperfusion, near infrared spectrometer (NIRS), and Doppler ultrasound. These conditions require emergent vascular surgery assessment and intervention.

V-A ECMO specific complications are differential oxygenation, left-ventricular distension, and cardiac and systemic thromboembolism. The retrograde arterial flow, particularly in peripheral V-A ECMO, increases the left ventricular afterload and impairs its drainage. As a result, cause left ventricular distension, stagnation of the blood, and backflow into the lungs. The left ventricular distension cause increase of the wall stress and could hinder left ventricular recovery [27]. The stasis of the blood can cause intra and extra-cardiac thrombi. In a retrospective analysis, the authors showed that 4% of patients on femoral V-A ECMO developed intra and extra-cardiac thrombosis despite adequate anticoagulation [28]. Another potential complication with V-A ECMO is the North-South syndrome or the Harlequin syndrome. It is characterized by lower oxygen saturation in the upper right extremity, cerebral, and coronary blood supply in comparison to the lower part of the body. It is best monitored by examining the blood from the right upper extremity or cerebral NIRS [29].

## **3.4 Prevention of complications**

The staffing model adopted by different institutions has the most impact on the ECMO patients' outcome and plays a major role in prevention of complications. ECMO specialist has the knowledge to understand the patient-circuit interaction, conduct frequent surveillance to prevent complications, and equipped to manage circuit emergencies. There is institutional variation in the staffing model due to the available resources and staffing capabilities. In an international survey of 177 ECMO centers, most institutions adopt 24/7 ECMO nurse specialist at 1:1 ratio with backup from perfusionists [30]. The ECMO specialist works collaboratively with the bedside nurse to ensure safe care for the critically ill patients with multiple organ dysfunction.

Usually, patients supported by ECMO do not require sedation during the ECMO run. There are multiple benefits associated with being awake while on ECMO support. For instance, ability to communicate, engaged in decision making, participate in active physical activity, and elimination of side effects of sedatives with delirium being the most prominent one [31]. We understand it might not be feasible for some patient populations, however having a timeline to achieve these goals is important. Patients might need to be sedated immediately after ECMO initiation, to ensure hemodynamic stability and proper gas exchange. Afterwards, gradual weaning of sedation is advised [32].

## **4. Emerging indications for extracorporeal membrane oxygenation**

There are many operative indications for ECMO that can be categorized based on the required support and modality (**Table 2**).

#### **4.1 Anticipated difficult airway**

ECMO can be used in patients with anatomically difficult airways, especially at or below the level of glottis, such as in patients with near complete tracheal


*Extracorporeal Membrane Oxygenation: Beyond Conventional Indications DOI: http://dx.doi.org/10.5772/intechopen.107883*


**Table 2.**

*Some of the indications for extracorporeal membrane oxygenation (ECMO) in the operative setting.*

obstruction [33]. Induction of general anesthesia leads to the loss of the respiratory muscle tone and collapse of the airway [34]. In some situations, bag mask ventilation and positive end expiratory pressure (PEEP) are ineffective to maintain oxygenation and ventilation. In a systematic review of literature from 1976 to 2017, 45 patients were placed on ECLS for critical airway diseases [35] pre-induction, with 18 patients placed on V-V ECMO, two patients on V-A ECMO, and 24 patients on cardiopulmonary bypass; one patient did not have a support mode not specified. The airway pathologies ranged from tracheal tumors, tracheal stenosis, and head and neck cancers. All patients survived to hospital discharge without significant complications.

#### **4.2 Complex airway surgeries**

ECMO facilitates complex tracheobronchial resection surgeries by providing adequate ventilation, hemodynamic support, (in the case of V-A ECMO) and allowing proper surgical exposure. In a single center, retrospective analysis of 10 patients who underwent complex tracheobronchial reconstructions on peripheral V-A ECMO, complete resection was accomplished in 8 patients with no perioperative mortality [36]. Another retrospective analysis highlighted 19 patients supported via V-V ECMO during malignant mass removal requiring rigid bronchoscopy and insertion of tracheal stents. V-V ECMO was weaned successfully in 18 patients, with one patient dying from massive bleeding [37]. Finally, there are multiple case reports that describe utilizing ECLS as an adjunctive intervention in the endoscopic removal of tracheal papillomas and repair of tracheobronchial fistulas [38, 39]. Use of ECMO to prevent any instrumentation of the airways without need for intubation is also described.

#### **4.3 General thoracic surgeries**

ECMO is a reasonable alternative for selective lung ventilation when it is difficult or not possible. Selective lung ventilation is usually required in tracheobronchial surgeries or single-lung surgery. In a retrospective questionnaire of 34 centers in France from 2009 to 2012, 36 patients required ECMO support during surgery (16 V-A and 20 V-V ECMO) [40]. Patients were divided into three groups (complete respiratory support, partial support, and patients with ARDS on ECMO preoperatively). The survival at 30-days were 7%, 40%, and 67% respectively. The authors concluded that ECMO is a valid alternative for in-field ventilation, with the outcome depending on preoperative respiratory status of the patient. In addition, there have been many reports regarding the use of ECMO in lung volume reduction surgeries [41]. These reports must be interpreted in the context of the outcome for such surgeries.

## **4.4 Lung transplantation**

ECMO is used at various stages in patients who require lung transplantation (bridge to transplant, intra-operatively, and post-transplantation in the case of primary graft dysfunction). The primary aim for ECMO as a bridge to transplant is to provide adequate gas exchange while maintaining the patient's functional status, with dual-lumen cannula V-V ECMO ideal for that goal. The presence of pulmonary hypertension can require assessment for other configurations such as V-PA or V-A ECMO to offload from the dysfunctional right ventricle. In a single-center study of 72 patients receiving ECMO as a bridge to lung transplantation, 42 patients received lung transplant from which 92.5% survived to hospital discharge and 84% survived at 2-years post-transplantation [42].

Intra-operatively, V-A ECMO is preferred over conventional cardiopulmonary bypass (CPB). V-A ECMO use is associated with a lower incidence of acute renal failure requiring dialysis post-transplantation, lower risk of bleeding, less requirement for blood transfusion, less incidence of primary graft dysfunction, shorter intensive care unit (ICU) and hospital length of stay [43, 44]. Post-lung transplantation, ECMO is used for primary graft dysfunction. The choice of which modality depends on the presence of associated pulmonary hypertension. In absence of pulmonary hypertension, V-V ECMO can provide the required support and the configuration is subject to the anticipated patient needs. However, if the patient has pulmonary hypertension, those patients are better served with V-A ECMO, V-PA, or hybrid configuration. In a single-center study of 58 patients required ECMO support for primary graft dysfunction, the survival rate was 58% at 30-days. There was no difference between V-V and V-A ECMO outcomes [45].

#### **4.5 Severe trauma victims**

There are multiple indications for ECMO in chest trauma patients. V-A ECMO can be used in patients with cardiopulmonary failure such as myocardial contusion, myocarditis, cardiac ischemia, and massive pulmonary embolism. On the other hand, V-V ECMO is used in lung contusions, or severe ARDS [46]. In a systematic review of 58 articles analyzing a total of 548 trauma patients who required ECMO support [47] the overall in-hospital mortality was 30.3%. Most of those patients (71.3%) received V-V ECMO and 24.5% were supported through V-A ECMO. Only 60% of the patients received systemic anticoagulation, 22.9% had hemorrhagic complications, and 19% experienced thrombotic events.

## **4.6 Liver transplantation**

ECMO has been used in the setting of orthotopic liver transplantation. Patients with liver failure are at risk for ARDS either before or after liver transplantation. The successful use of V-V ECMO in the pre-transplant setting has been described in the literature but it is unclear if it is a contraindication for liver transplantation [48], considering that the presence of mechanical ventilation and moderate ARDS is associated with poor outcomes in this patient population [49]. One of the major challenges

*Extracorporeal Membrane Oxygenation: Beyond Conventional Indications DOI: http://dx.doi.org/10.5772/intechopen.107883*

with these patients is anticoagulation management since they are coagulopathic due to the underlying liver dysfunction and ECMO-related coagulopathy is an added layer of risk and complexity. More commonly, ECMO has been used after liver transplantation in the form of V-V ECMO to overcome hepato-pulmonary syndrome or pulmonary infection; additionally, liver transplantation induces pulmonary remodeling, causing ventilation/perfusion mismatch that may require V-V ECMO support. Some patients post transplantation may also be supported with V-A ECMO, such as when they develop hemodynamic compromise in the setting of pulmonary embolism or right ventricular failure [50, 51]. Also, because liver transplantation patients are predisposed to right ventricular failure which could cause hepatic congestion and impair the freshly transplanted liver, V-A ECMO can facilitate decompression of the right ventricle, supporting the transplanted organ. In a recent case series of eight liver transplantation patients requiring ECMO support, 38% survived to hospital discharge [52]. However, utilization of ECMO in liver transplantation patients remains a challenge given the hematological, hemodynamic, and the immunological profile of this patient population.

### **4.7 Massive pulmonary embolism**

Massive pulmonary embolism is associated with poor survival because of its association with obstructive shock, end-organ dysfunction, and cardiac arrest. High-risk pulmonary embolism is defined as persistent hypotension (systolic blood pressure less than 90 mmHg, drop in systolic blood pressure more than 40 mmHg, and the need for vasopressors for more than 15 min) despite resuscitation [53, 54]. Systemic thrombolysis and anticoagulation remain the first line therapy for high-risk pulmonary embolism. However, this can be associated with increased risk of bleeding including intracranial hemorrhage especially in the elderly patients with multiple co-morbidities [55]. When systemic thrombolysis is contraindicated, V-A ECMO can provide perfusion to the end-organs. Also, the use of systemic anticoagulation can mitigate the need for systemic thrombolysis by allowing time for endogenous thrombolytics to act [56]. V-A ECMO can also be used in scenarios when thrombolytics fail, for hemodynamic support before intervention, refractory cardiogenic shock, or cardiac arrest [57]. In a study of 59 patients with massive pulmonary embolism, 29 patients were treated by surgical embolectomy and 27 patients were placed on V-A ECMO with systemic anticoagulation with or without subsequent surgical embolectomy. One year survival was significantly higher in the ECMO group (96%) versus the control group (73%) [58].

#### **4.8 Extracorporeal cardiopulmonary resuscitation (ECPR)**

ECPR is defined as the initiation of ECMO when CPR is ongoing (i.e., the patient does not achieve return of spontaneous circulation prior to going on ECMO). There are multiple patient populations that could benefit from ECPR, such as patients who arrest from cardiomyopathy, right ventricular dysfunction, and massive pulmonary embolism. Induction of anesthesia and intubation place those patients at higher risk of cardiac arrest. The best predictors for favorable neurological outcome in these patients, like patients who sustain a cardiac arrest, include witnessed cardiac arrest, immediate initiation of chest compressions, shockable rhythm, cardiac arrest due to a reversible etiology, and low flow time of less than 60 min [59, 60]. The longer the time to ECMO, the less the benefit of ECPR [61]. In a retrospective comparison of ECPR

for in-hospital cardiac arrest to conventional CPR, ECPR led to favorable neurological outcome at 3 months [62]. Use of ECPR in out of hospital arrest is also becoming of increasing use and descriptions of both on-site ECPR implementation and that using a specific algorithm to apply emergently once the patient arrives to the hospital have shown some success [63, 64].

## **4.9 ECMO during pregnancy**

The increased use of ECMO in pregnant patients is attributed to increasing rates of cardiogenic shock in the peripartum period [65]. The presence of cardiogenic shock is associated with 18.81% of maternal mortality and usually leads to adverse events such as cardiac arrest and intrauterine fetal death. Similarly, the presence of severe ARDS in this patient population is associated with increased maternal mortality and fetal asphyxia [66]. V-A ECMO successfully provides the necessary circulatory support until the heart recovers. Also, it has been used as rescue intervention in pregnant patients with a massive pulmonary embolism, amniotic fluid embolism and maternal pulmonary hypertension [67]. V-V ECMO in patients with severe ARDS provides the necessary gas exchange when the patient's native lungs are inadequate due to increased intra-abdominal pressures in pregnancy [68]; further, it allows using ultraprotective lung settings, reducing ventilator induced lung injury.

In an analysis of the ELSO data between 1997 and 2017, the overall survival for pregnant patients who are supported on ECMO was 70%. There was no difference in the outcome between both V-V and V-A ECMO [69]. Pregnant patients who required ECPR had the same survival rate that is comparable to non-pregnant ones (54.8% versus 58%) [70].

## **4.10 High-risk cardiac procedures**

Refractory ventricular tachycardia (VT) is associated with hemodynamic instability in the form of progressive cardiogenic shock, and even cardiac arrest [71]. Urgent VT ablation is required if the patient fails to respond to antiarrhythmics, intubation, heavy sedation, and neuromuscular blockade. Performing VT ablation on a hemodynamically unstable patient is challenging; additionally, VT ablation can exacerbate the underlying instability and worsen outcomes [72]. V-A ECMO can provide the required circulatory support before and during a VT ablation procedure. In terms of outcomes, one study, which was a systematic review of all patients that were placed on V-A ECMO for periprocedural VT ablation, showed short-term mortality of 15% and all-cause mortality at longest follow-up at 25% [73]. The most common causes of death were refractory VT, cardiac arrest, and acute heart failure. The duration of V-A ECMO support ranged from 140 min to 6 days. This study, among others, highlighted the role of V-A ECMO in refractory VT patients, and described that further data is needed on appropriate patient selection, outcomes, and procedural optimization. For patients with refractory arrhythmia, implementation of ECMO may improve myocardial oxygenation and normal rhythm may result.

Another use for V-A ECMO is in high-risk percutaneous coronary intervention (PCI). High-risk PCI carries an increased incidence of morbidity and mortality during and after the procedure. There are multiple risk factors for high-risk PCI, which include patient characteristics such as age, diabetes mellitus, chronic kidney disease, prior myocardial infarction, peripheral vascular disease, signs of heart failure and left ventricular function [74]. Other risk factors include the presence of multi-vessel *Extracorporeal Membrane Oxygenation: Beyond Conventional Indications DOI: http://dx.doi.org/10.5772/intechopen.107883*

disease, left main disease, and a saphenous vein graft lesion. PCI can induce transient myocardial ischemia that is not well-tolerated in the high-risk patients. V-A ECMO has the advantage of providing adequate biventricular support that can reach more than 5 LPM. In addition, it can be quickly deployed at bedside in the event of significant hemodynamic compromise or cardiac arrest. In certain circumstances, it can be initiated prior to high-risk PCI; in a case series of a single center experience, five patients were placed on ECMO in preparation for high-risk PCI. All patients tolerated their procedure and four of them were weaned off ECMO in less than 24 hours [75].

#### **4.11 Extracorporeal membrane oxygenation during coronavirus 2019 pandemic**

The role of extracorporeal membrane oxygenation (ECMO) in Coronavirus 2019 (COVID-19) associated severe acute respiratory distress syndrome (ARDS) has been a subject of debate because of the early negative results [76, 77]. Despite that ECMO has been recommended as supportive intervention by multiple societies [78, 79]. However, subsequent studies from the extracorporeal life support organization (ELSO) showed that the use of V-V ECMO in COVID-19 is associated with an in-hospital mortality of 36.9–51.9% at 90 days [80, 81]. Similarly, in a French retrospective single healthcare system analysis, the estimated probability of death at 60 days post-ECMO initiation was 31% [82]. Most recently, in a comparative analysis of COVID Critical Care Consortium, the use of V-V ECMO in comparison to mechanical ventilation only was associated with a significantly reduced mortality especially in patients less than 65 years old and with a PaO2/FiO2 < 80 mm Hg or with driving pressures >15 cmH2O during the first 10 days of mechanical ventilation [83].

## **5. Transportation of patients on extracorporeal membrane oxygenation (ECMO)**

While the transportation of patients on ECMO is usually minimized, it commonly must occur—for instance, when the patient is placed on ECMO in the Operating Room, the Emergency Department, or a different center, and requires transportation back to the ICU, or specific imaging or catheterization is required for the patient. Thus, establishing a systematic approach and becoming comfortable with the transport of patients on ECMO is an important component in any ECMO center. Some studies report the rate of complications associated with ECMO transport close to 30% [76], with most of the complications being patient related. Having a dedicated multi-disciplinary team with assigned roles and responsibilities is the first step in the process [77] to achieving safer transports. The team usually includes the ECMO specialist, with their primary focus being on the equipment function and connection, the critical care nurses who manage infusions and monitor patient vitals, the respiratory therapist who is responsible for the mechanical ventilation, and the physician who focuses on the continuous monitoring of the patient/their vitals. The roles of different team members may appear isolated but is mutual and overlapping. Transport teams which do not require as many team members, especially if the patient is already cannulated, can also be successful if experienced. Physician physical presence can also be provided remotely but medical oversight to the team should be provided. Clear, closed loop communication is an important aspect throughout. The best method to train the transport team is by conducting simulation scenarios to address the most

common complications that could arise [78]. ECMO centers are highly encouraged to develop ECMO transport checklists aimed at minimizing the near misses and reduce human-factor error. The literature and ELSO guidelines have many examples that could be adopted by different institutions [77, 79]. Both hospitals based and private ECMO transport teams exist.

## **6. Weaning of extracorporeal membrane oxygenation**

Readiness for discontinuation of ECMO is determined by the degree of heart and lung recovery. In V-V ECMO, the resolution of the lung pathology as evident by improvement of lung compliance, resolution of the lung pathology on chest imaging, and adequate gas exchange without ECMO support [80]. The adequacy of gas-exchange is usually assessed by turning of the sweep gas for at least 24-hours. If adequate oxygenation (PaO2/FiO2 ratio > 150), and ventilation is maintained with acceptable patient respiratory effort, V-V ECMO can be removed. In the V-A ECMO, cardiac recovery is assessed by stable hemodynamics and vasoactive medication doses on decreasing the V-A ECMO flow [81]. Echocardiography is crucial part of assessing the heart right and left ventricular function before decannulation of the V-A ECMO, which can be done in the operating room or bedside based on the institution experience.

## **7. Discussion**

Our review highlighted some of the indications for ECMO in acute care setting. These indications represent the expansion and familiarity by the ECMO advanced technology. Barbaro et al. demonstrated that the annual extracorporeal membrane oxygenation (ECMO) patient volume has a potential impact on case-mix–adjusted hospital mortality rate for patients supported by ECMO [3]. However, a recent paper challenged this observation and did not show an associated between the hospital volume and the ECMO outcome [82]. ECMO is resource intensive technology and that might limit its use [83]. To overcome these limitations, it is important to establish an organization of ECMO centers internally and externally (in the same region or country) to optimize the cost-effectiveness. Internal organization, based on the importance of establishing protocols, investing in the technology and education. Also, having multi-disciplinary team that actively participate in decision making, reviewing the patient outcomes based on preidentified quality indicators. External organization is based on coordination of care among the ECMO centers in the same region to refer patients based on specific center expertise and resource availability [84].

Despite the expansion of ECMO use, there are variation in the selection of patients who will benefit the most of this technology. Most of the selection criteria are based on the anticipated duration of support and the likelihood of weaning of ECMO support. Hence the decision is based mostly on the local institution experience, especially in the light of absence of rigorous clinical evidence. Utilization of mortality prediction score such as Survival after Veno-Arterial ECMO (SAVE) score and Respiratory ECMO Survival Prediction (RESP) score, could be helpful in decision making and informing the caregivers regarding the potential clinical outcomes [85, 86].

*Extracorporeal Membrane Oxygenation: Beyond Conventional Indications DOI: http://dx.doi.org/10.5772/intechopen.107883*

## **8. Conclusion**

In conclusion, the expansion of ECMO use and technology has created new opportunities for its utilization beyond the conventional indications for ECMO. The robust evidence for each indication is still lacking. However, the early deployment of ECMO in high-risk cases for cardiac and respiratory failure is important before the patient experiences a massive complication such as cardiac arrest. Similarly, this advanced supportive technology is associated with known complications and requires extensive expertise to manage patients on ECMO. Hence the need for expanding the clinical and scientific knowledge to delineate the best patient's population with might benefit from ECMO, in context of the best structure and staffing of the ECMO programs. The decision to place a patient on ECMO must be discussed with a multidisciplinary team weighing the risks and the benefits.

## **Author details**

Akram M. Zaaqoq1 \*, Mariam Gabrial<sup>2</sup> and Heidi J. Dalton2

1 Department of Critical Care Medicine, MedStar Washington Hospital Center, Georgetown University, Washington, DC, USA

2 Department of Pediatrics, Inova Fairfax Hospital, Falls Church, VA, USA

\*Address all correspondence to: akramzaaqoq@gmail.com

© 2022 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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## **Chapter 6**

## Anesthesia for Non-Cardiac Surgery for the LVAD Patient

*Kathryn Foster and Steven S. Silvonek*

## **Abstract**

Heart failure is poorly tolerated and end stage heart failure (classified as New York Heart Association (NYHA) class IV) has a two-year survival with medical therapy that approaches 0%. Innovation in this sphere has yielded mechanical therapies, principally the left ventricular assist device (LVAD). In the last decade one-year survival rates of Left ventricular assist device patients have increased from 52–83%. As this therapy is more commonly used to treat advanced heart failure, coupled with the increase in patient survival after implantation, patients are increasingly encountered in the peri-operative arena requiring anesthesia for non-cardiac surgeries. The goal of this chapter is to provide the non-cardiac trained anesthesia provider a primer on what an LVAD is, how it functions, the physiological changes that occur with implantation, and considerations for administering anesthesia to patients with LVADs for non-cardiac surgery. Review of articles from 2018 to 2022 found from a search on PubMed and Google Scholar using the keywords: "Left Ventricular Assist Device", "LVAD", "anesthesia", "non-cardiac surgery", "Doppler blood pressure measurement", "VAD coordinator". Non-cardiac trained anesthesia providers can safely administer the anesthetics to LVAD patients undergoing non-cardiac surgery as long as appropriate considerations are taken.

**Keywords:** anesthesia, left ventricular assist device, LVAD, non cardiac surgery, blood pressure measurement

## **1. Introduction**

Cardiovascular disease continues to be the leading cause of death in America. Around six million Americans are diagnosed with heart failure of varying degrees each year [1–5]. Left Ventricular Assist Devices are indicated for patients with advanced stage heart failure. Medical optimization can include renin angiotensinaldosterone system antagonists, sympathetic nervous system antagonists, beta blockers [1, 4–8]. Cardiac resynchronization therapy is often used in chronic heart failure candidates to stave off final implantation [1, 4–8]. In end-stage heart failure, conventional medical therapies have a mortality at 2 years of almost 100% [9]. These patients are classified NYHA class IV or Stage D by the American College of Cardiology Foundation/American Heart Association. Clinically, they have shortness of breath at rest and their echo shows an ejection fraction (EF) of 40% or less. While cardiac transplant is a definitive treatment for severe advanced heart failure and may be the preferred treatment, this solution is limited by donor availability. The failure


#### **Table 1.**

*Indications of LVAD therapy [4, 5, 8, 11, 14, 15].*

of medical management, the shortage of heart donors, and the realization that these patients were not suitable transplant candidates led to the development of the LVAD [2, 4, 5, 10–12].

The first LVADs were used in the 1960s as bridge to therapy (BTT), or as a bridge to recovery (BTR) [2, 4, 5, 8]. Initially, they were designed to emulate the pulsatile action of the heart, had many moving parts and membranes, and were prone to frequent failure. After improvements in portability and mechanical design, the latest generation of devices are all continuous. By 2010, LVADs were approved for destination therapy (DT). As of 2020 destination therapy accounts for 78% of LVAD implantations in the US [13]. **Table 1** describes indications for LVAD therapy.

The evolution of the LVAD devices is a nascent, growing field and improvement to its models was rapid: In 2009, the one-year survival rate of an LVAD patient was 52%. By 2018, the one-year survival rate after an LVAD implant increased to over 80%; the two-year survival was above 70%; some patients lived 4 years or more [1–5, 7, 16–19]. As patients with these devices live longer, they may experience complications or other medical conditions that require surgical intervention and therefore anesthesia. One early review of Medicare patients found that in 2012, 64 LVAD patients had non-cardiac surgery (NCS) and that number increased in 2017 to 304 LVAD patients [7]. No doubt the number now is far higher in the 2020s. As more patients with these devices present for non-cardiac surgery, it is important for anesthesia providers to understand the hemodynamic and physiologic changes that result from LVAD placement and how our anesthetic techniques and medications affect its function [6, 20].

## **2. The LVAD**

The current LVAD is a rotary continuous pump system that is implanted at the apex of the left ventricle and propels blood into the aorta via an outflow graft, typically to the ascending aorta. **Figure 1** shows a basic silhouette of the Heart Mate III, now the most implanted device of the 2020s [1].

The pump receives energy from a driveline that connects extracorporeally to a battery system through a controller when on battery power [1, 3, 11]. This device is so compact, the functional parts fit completely inside the thoracic cavity. The drive train can also be attached to a wall unit for power and with a larger display screen.

#### **2.1 First generation devices**

The first generation of LVADs were pulsatile and large [4, 16]. The Thoratec PVAD was the first LVAD to be approved by the Food and Drug Administration. It was used

*Anesthesia for Non-Cardiac Surgery for the LVAD Patient DOI: http://dx.doi.org/10.5772/intechopen.111491*

#### **Figure 1.**

*The silhouette of the heart mate III components, the most implanted device of the 2020s. (a) Centrifugal pump (b) driveline cable (c) controller panel (d) portable battery [1].*

in more than four thousand patients as a bridge to transplant [4]. Its pump was not implanted but had to be carried extracorporeally [16].

The Novacor and HeartMate I (HM I) became the first implantable LVADs. **Figure 2** shows an image of a HeartMate I device and its parts. The pumps of these devices were implanted in a preperitoneal pocket under the abdominal muscles. The Novacor had great durability, lasting for 5–6 years. However, the rate of stroke among its users was near 50% [1]. The HM1 device attempted to recreate physiologic pulsatile flow and was used as a BTT and BTR for more than two decades [4, 16]. The HM I had a 52% one-year survival rate, 48% better results than medical management at those times. Unfortunately, it was mechanically complex, was prone to malfunction, and also had high rates of severe adverse events and infection. The device was trialed for Destination Therapy (DT) but ultimately failed, as it was deemed not ideal and its parts wore out at about 18 months [1, 4].

#### **2.2 Second generation devices**

The HeartMate II (HM2) device was introduced in 2008 (**Figure 3**) [4]. It is considered a second-generation device because it delivers continuous flow (CF)

**Figure 2.** *The HeartMate 1 [3].*

powered by an axial flow rotor propeller. The pump of the HM2 is 1/7th the size of the HM I [21], about the size of a D battery but is similarly implanted in a preperitoneal pocket [1, 16]. The HM2 boasted a 68% one-year survival rate with improved quality of life and physical activity noted at 3 months post implantation [4]. It achieved a 58% two-year survival rate compared to the HeartMate I (24%) in the 2010 REMATCH trial.

The HM II was the first device approved for destination therapy (DT) [2, 4, 15, 16, 18]. Rates of stroke, bleeding, infection, and device malfunction were less than its predecessors [1, 4]. With advances in implantation technique, design, and RV support devices, DT patients were approaching a 70% two-year survival rate, with one patient documented to have their HM2 for greater than 8 years [1, 7, 17]. However, the HM2 had its own unique complications related to its continuous axial flow.

Patients with HM2 unfortunately would present with pump thrombus. As a result, use of systemic anticoagulation, such as with warfarin, became a standard for all LVAD patients in 2011 [1]. Acquired von Willebrand deficiency and arteriovenous malformations (AVM) developed related to altered physiology associated with continuous flow LVADs. When combined with prophylactic anticoagulation, the incidence of gastrointestinal bleeding rose [1, 2, 4, 10, 11, 16].

## **2.3 Third generation devices**

Second generation CF devices improved longevity compared to first generation but had multiple moving parts. Third generation CF devices, such as the Heart Mate *Anesthesia for Non-Cardiac Surgery for the LVAD Patient DOI: http://dx.doi.org/10.5772/intechopen.111491*

**Figure 3.** *The heart mate II [4].*

III and the HeartWare HVAD, are positioned at the apex of the left ventricle blood pumps blood in a centrifugal manner [1, 4, 16]. Both devices are smaller than their predecessors. They have also shown greater longevity with significantly less need for reimplantation than the HM2 [1, 4, 5].

## **2.4 HVAD**

The Medtronics HeartWare HVAD (**Figure 4**) was approved by FDA in November of 2012 for BTT. It has been implanted in more than 20,000 heart failure patients worldwide, with one HVAD being implanted for greater than 7 years [1, 22]. The HVAD functions via both passive magnetic levitation and a hydrodynamic bearing system [22]. In June of 2021, the sale and implantation of the HVAD was discontinued secondary to technical issues with the device not restarting after planned or accidental power disconnection. The HVAD patients also held a statistically significant incidence of stroke [12, 22]. About 4000 patients worldwide still have HVADs implanted. As a result, Society of Thoracic Surgeons recommends explantation of the HVAD to HM3 only in instances of malfunction, as electively changing devices carries just as much risk as keeping the HVAD [11, 22].

**Figure 4.** *The internal components of the Heartware HVAD [4].*

## **2.5 HeartMate III**

The Abbott HeartMate III system is a completely magnetically levitated centrifugal pump (**Figures 1** and **5**) [1, 4, 16, 22]. The centrifugal flow of the HM3 not only improves longevity of the devices but produces less shear on blood components. This has resulted in milder acquired von Willebrand syndrome. Other adverse events such as pump thrombus, stroke, and GI bleeding are decreased in HM3 compared to HM2 [1, 4, 5, 17, 23]. HM3 patients also spend less days in the hospital 2 years post implant [17]. Unfortunately, rates of right heart failure and infection with third generation devices remain similar to previous generations [1, 4, 17].

## **2.6 External components of the LVAD**

**Figure 6** shows an example of a Heartmate III controller. The controller contains a screen that displays four values: pump speed (rotations/minute), pump flow (liters/ min), pulsatility index (PI), and pump power (watts) [3, 11, 16]. When in the OR

*Anesthesia for Non-Cardiac Surgery for the LVAD Patient DOI: http://dx.doi.org/10.5772/intechopen.111491*

**Figure 5.** *The internal components of the HeartMate 3 [4].*

#### **Figure 6.**

*Controller panel of the HeartMate 3. (A) LVAD controller panel and (B) panel of indicator lights [3].*

and connected to wall power, a larger monitor can be fashioned to display all values concurrently.

Pump speed shows how fast the LVAD centrifuge is spinning and is the only directly modifiable value of the LVAD. Pump speed can be adjusted to optimize function under visualizaiton with echocardiogram. Pump flow is analogous to cardiac output and is different for each model; this value is typically a derived number calculated with proprietary formulas [16, 24].

Pump power is indicative of how much power is being required to run the pump at a specific set pump speed. In its normal function, this value varies linearly with systemic vascular resistance.

Pump flow is therefore a calculated value from pump power. Changes and trends of the pump flow value can also indicate complications. For example, any increase in power not related to an increase in actual flow will cause an erroneously high flow to read, such as the presence of a thrombus in the inflow cannula.

The pulsatility index is the difference of systolic and diastolic pressure within the pump system. Its magnitude reflects the amount of assistance provided by the LVAD; when the left ventricle contracts, the PI increases the flow transiently in the LVAD. This value is key to interpreting Doppler blood pressures (DopBP), which will be discussed later in this chapter [16, 19, 25].

**Table 2** displays normal values for the three continuous flow LVADs currently in use or available for implantation [3, 11, 18, 24]. Since the LVAD is essentially a conduit bypassing the left ventricle, it is entirely possible that the aortic valve does not routinely open. Any pulsatility that does occur is not the result of ventricular ejection through the aortic valve, per se. It is actually the result of any residual left ventricular function that with each beat provides an increase in preload to the LVAD, resulting in a transiently higher flow. The newest LVAD devices, including the HM III, routinely cycle their RPMs transiently higher and lower than their set value instead of remaining static, thus creating more pulsatility than their predecessors. This decreases the incidence of AVMs which often are responsible for GI bleeding.

Many factors can affect physiologic LVAD pump function, including hypovolemia, anesthetic agents, surgical positioning and technique. **Figure 7** is a flow diagram of changes in pump values that may indicate different physiologic states when the pump flow is increased. Patients with high pump flows and low PI values may be indicative of vasodilation, aortic valve regurgitation, or high pump speed. Of the three, vasodilation is the most likely cause related to anesthesia and should be treated with titration of vasopressors, inotropes, and intravenous fluids. If the pump flow is high and the PI is increased, then the patient may be hypervolemic or have increased myocardial contractility, such as with inotrope usage [3, 12, 24]. **Figure 8** details a flow diagram to help interpret changes when the pump flow is decreased. Low pump flow with high PI can be caused by hypertension, decreased VAD speed, or partial outflow obstruction from the outflow cannula. Of the three, hypertension is the cause most likely associated with an anesthetic. Titrating antihypertensives, administering pain medication, or increasing depth of anesthesia are ways to address these changes. If pump flow and PI are both low, this may indicate partial inflow obstruction or low


**Table 2.**

*Normal value ranges of LVAD devices for speed (rotations per minute (rpm)), flow, and power [3, 10, 18, 24].*

*Anesthesia for Non-Cardiac Surgery for the LVAD Patient DOI: http://dx.doi.org/10.5772/intechopen.111491*

**Figure 7.** *Flow diagram for interpreting changes in LVAD function with increased flow [12, 24].*

**Figure 8.**

*Flow diagram for interpreting changes in LVAD function decreased flow [12, 24].*

preload secondary to hypovolemia, right sided heart failure, or cardiac tamponade. In the setting of an anesthetic, hypovolemia is most likely the cause of this pattern and can be treated with titration of a fluid bolus [3, 12, 24].

## **3. Complications of LVAD device**

The most common complications with continuous flow LVADs are right ventricular (RV) failure, gastrointestinal (GI) bleeding, infection, pump thrombus, stroke, and ventricular arrhythmias [3, 4, 11, 14, 17, 23].

## **3.1 Right ventricular failure**

RV failure is noted in about 35%- 40% of LVAD patients. This may present acutely right after implantation or is a delayed phenomenon attributed to increased preload, septal shift, and less contractility [4, 6, 12, 14, 17]. 10–25% of LVAD patients will require RV support as a poorly functioning RV limits the LVAD system by way of preload [6, 14]. Supportive measures may include a variety of modalities such as lusitropic medications, diuretics, and pulmonary vasodilators [11, 12]. Patients who are refractory to medical management may require a right ventricular assist device (RVAD) or in some cases total artificial heart [4].

## **3.2 Gastrointestinal bleeding**

GI bleeds occur in around 30% of patients with LVADs [2, 8, 16–18]. Upper GI bleeds are more common than lower GI bleeds [3, 11]. The most common source of bleeding is arterial venous malformations, the formation of which is attributed to lack of arterial pulsatility and acquired von.

Willebrand disease [1, 2, 4, 10, 11, 16, 26]. Interestingly, the HM III is thought to partially mitigate this by cycling its RPMs (revolutions per minute), thus creating a partially pulsatile state. Patients with history of gastric ulcers, colon polyps, and hx blood thinner use prior to LVAD placement are at higher risk for developing GI bleeds [4]. The requirement of anti-coagulation, typically with coumadin targeting an INR of 1.5–3, as well as aspirin, also exacerbate the bleeding risk [2, 4, 10, 16]. **Figure 9** provides a visual for how these factors contribute to GI bleeds.

#### **Figure 9.**

*Factors of continuous flow (CF) LVADs that contribute to GI bleeding [2].*

## *Anesthesia for Non-Cardiac Surgery for the LVAD Patient DOI: http://dx.doi.org/10.5772/intechopen.111491*

Acute management of GI bleeding will likely include a combination of holding anticoagulation/antiplatelet medications, providing octreotide, and performing an endoscopy exam [2, 11, 12]. Holding anticoagulation has shown to be safe for short periods of time and should be restarted slowly with a lowered INR goal after signs of bleeding have stopped [2, 4, 15, 16]. Octreotide is a somatostatin analog that functions by decreasing gastric secretions that prevent clot formation [12]. Endoscopies require anesthesia and diagnose the source of bleeding in 1/3 of patients. In cases of severe GI bleed, reversal of anticoagulation with vitamin K or fresh frozen plasma may be used. Von Willebrand factor may also be administered [2, 12]. If the source of bleeding is not identified and bleeding continues, angiography may be attempted to identify and embolize source vessels [11]. Maintaining lower doses of anticoagulants may be used as long-term treatment and prevention of GI bleeding [12].

## **3.3 Infection**

Infection can occur at surgical incisions or anywhere along the device system. Driveline infections are the most common, comprising 80% of LVAD associated infections [4, 12]. Any infection in the LVAD patient will be treated with hospital admission and intravenous antibiotics to prevent sepsis [12]. Driveline infections may also require surgical debridement in the operating room [12]. Explantation of the LVAD device with re-implantation is the final treatment if any components of the internal device become infected [4, 10]. Self-care education of LVAD users is key to prevention of infection. Lifelong antibiotic suppressive therapy is an alternative for those who are too high a surgical risk. Using techniques such as anchoring the driveline near the skin and using a silver dressing have shown to decrease infections in a small study [12].

## **3.4 Pump thrombus**

Pump thrombus is a complication unique to continuous flow LVADs. HM3 has the least incidence of suspected pump thrombus; less than 3% at the two-year post implantation mark [4, 12, 17]. Thrombus can occur anywhere within the pump. A thrombus in the inflow and outflow cannula may be seen on CT scan with contrast. Visualization of thrombus anywhere else within the system can only occur with explantation [12]. An elevated pump power with decreased pulsatility index will be noted on the controller screen of the LVAD [4]. Transthoracic or transesophageal echocardiogram may show a dilated left ventricle, mitral regurgitation, and aortic valve opening with systole [12]. Clinically, a palpable pulse may be felt secondary to aortic valve opening [2, 6]. Labs will show an increased lactic dehydrogenase and decreased hemoglobin when suspecting LVAD pump thrombus [12]. In 50% of less severe cases, the patient will successfully be treated with heparin and inotropes [14]. In severe cases where pump thrombus treatment is refractory to medical management, the pump is exchanged as definitive treatment [4, 10]. Strategies such as maintaining INR 2–2.5 with warfarin, daily aspirin, and mid-range pump speeds decrease thrombus rates significantly. The PREVENT study saw a decrease in thrombus rates from 8.9 to 1.9% by implementing the following strategies: coumadin to keep INR 2–2.5, daily aspirin, and pump speeds greater than 9000 RPMs (for HM II) [3, 4, 14].

#### **3.5 Stroke**

There is an increased incidence of stroke associated with pump thrombus and mean arterial pressure (MAP) greater than 90 mmHg. For LVAD patients, a MAP greater than 90 mmHg is considered HTN [3, 4, 11]. Data shows that about 9% of patients with an LVAD have a stroke within 34 months of implantation [12]. Favored treatment for ischemic strokes in the LVAD population is endovascular thrombectomy. Intravenous thrombolysis has not yet been tested sufficiently [3, 12]. The histology of clots is different in LVAD patients and clot retrieval devices require more passes of devices are typically required to alleviate ischemic strokes in LVAD patients vs. non-LVAD patients [27]. A decrease in stroke rates by two thirds was noted with adherence to the same regimen that decreased pump thrombus. The protocol includes maintaining mid-range pump speed, anticoagulation with warfarin to keep INR values 2–2.5, and daily aspirin [3, 4]. The newer generation HM3 has less incidence of stroke compared to the HMII [3, 4, 12].

#### **3.6 Ventricular arrhythmias**

Ventricular arrhythmias occur in about 15–34% of LVAD patients, with the highest incidence in the first 30 days post implantation. An average of 34% of LVAD patients have an episode of ventricular tachycardia within 1 year of implantation [4, 6, 16]. Many have an ICD implanted prior to LVAD implantation [4, 6, 10, 14, 16]. Ventricular arrhythmias may be caused by so-called "suck down" events: when the left ventricle has a low volume and collapses on itself [4, 6, 11, 16, 28].

Treatment is to slow the VAD speed to allow increased filling of the ventricle, and support with vasopressors [4, 6]. Management of ventricular arrhythmias and suction events will be discussed further in the Intraoperative management section of this chapter.

## **4. Perioperative considerations for LVAD patients undergoing non-cardiac surgery**

As people are living longer with LVADs, other health issues may arise that require surgical intervention and therefore the need for anesthesia [15, 20]. 15–20% of LVAD patients present for non-cardiac surgery (NCS), whether elective or urgent/emergent [7, 18]. In one study held in Europe from 2012 to 2019, within 60% of LVAD patients who had surgical interventions, 39% of procedures were unplanned and 61% were elective [18]. Over half of the patients required general anesthesia, whereas 5% of cases were performed under local [18]. A review of Medicare patients with LVADs in the United states within the same time period shows close to 75% of the non-cardiac surgery cases were unplanned and around 25% reported as elective [7]. Common procedures LVAD patients may undergo include treatment of GI bleeding, surgical debridement of skin infections, ICD generator changes, and emergent orthopedic and cystoscopy cases [7, 18]. Another report described the care of morbidly obese LVAD patients for laparoscopic sleeve gastrectomies, to improve transplant candidacy [29].

Ideally, surgical procedures involving an LVAD patient should take place at a medical center that implants LVADs. It is suggested that for any complex patients or larger surgeries that a cardiac anesthesiologist be the primary anesthetic provider. Many smaller procedures, sedation cases, and well-maintained patients may not necessitate the need for cardiac trained anesthesia providers [15, 16].

## **4.1 Surgical optimization during the pre admission testing and preoperative period**

The typical patient living with an LVAD may be in better physiological condition when compared with patients with severe heart failure not on LVAD therapy. Studies show that around 30–70% of non-cardiac surgery events in LVAD patients are electively scheduled [7, 11, 15, 18]. Efforts should be made to have an LVAD coordinator plan and organize care for these patients [30]. Duties include communicating and coordinating needs of the planned procedure, providing patient education, including anticoagulation management, organizing availability of LVAD staff and anesthesia, and setting up goals for postoperative care [16, 20].

Most elective and many unplanned procedures may not require a cardiac trained anesthesia provider [15, 16, 18]. However, it is suggested that both a CT surgeon and a cardiac anesthesiologist are aware of the patient having a procedure and be available for consultation. For LVAD patients that present with hemodynamic instability, it is recommended that a cardiac anesthesia team be present for surgery [16].

The type of anesthesia required is case dependent. However, ideally and whenever possible, cases should be performed under local, regional, or MAC [16]. Neuraxial anesthesia is not typically thought of an ideal modality for LVAD patients due in part to their requirement of systemic anticoagulation, but most troublesome is the profound vasodilation and subsequent abatement of preload that can rapidly lead to ventricular "suck down" phenomenon if not appropriately anticipated. In normalization of practice, it has been found that an epidural may even be provided to laboring women with LVADs [14]. General anesthesia can safely be administered in a patient with an LVAD, provided once again, one accounts for the frequent shifts in hemodynamics [20]. Discussing the type of anesthesia and the expected patient experience is important [16].

LVAD patients may need to be admitted 24–72 hours prior to scheduled procedure for heparin bridging and fluid optimization [16, 18, 20]. Management of anticoagulants will depend largely on the type of surgery and anticipated blood loss. Warfarin is most commonly stopped and bridged with heparin in hospital. Aspirin may be continued as the antiplatelet therapy has proven to be beneficial perioperatively [18, 20]. Fresh frozen plasma, prothrombin complex concentrate (PCC), and vitamin K can be used in emergent situations to reverse warfarin [3, 16, 18, 20]. In small cases with little to no anticipated blood loss, patients may be instructed to stop or decrease anticoagulation doses within a few days of scheduled procedure. Studies have shown that stopping or decreasing the dose of anticoagulation does not increase risk of adverse events [4, 15, 16].

Also understand that all LVAD patients have acquired von Willebrand's disease related to blood shearing forces that flow through the pump [4, 16]. Perioperative DDAVP may be indicated depending on the type of surgery. Actual use is quite low at 0.3% [26].

Fluid status is important given the dependency of LVAD to function well with adequate preload. A pre-op echocardiogram can be performed to ensure the most complete assessment of the patient's cardiac function, including RV function and to provide opportunities for fluid optimization.

Should a patient have an ICD, it is recommended that the device be interrogated and/or reprogrammed to accommodate surgery, especially in cases where electrocautery will be used [16]. The anesthesia provider should also assess the driveline location and be familiar with individual patients' pump and baseline parameters [16]. In

regards to physical examination, LVAD patients should not have a palpable pulse and heart sounds may not be elicited well upon auscultation, secondary to the hum of the.

LVAD device [3, 10, 11, 25]. In fact, a palpable pulse may indicate pump thrombus [3]. Setup and teamwork among the operating room staff members is important for an LVAD patient. The intended procedure should be reviewed, and all positioning and equipment needs considered and verified. Communication among all staff should be emphasized and the surgical team reminded of the sensitive hemodynamic state of an LVAD patient, for instance, during types of positioning or when viscera is manipulated [18]. Some positions may affect positioning of the inflow cannula and impede pump flow. Improper drive line cushioning could lead to pressure injury and tissue necrosis. For laparoscopic procedures, insufflation of abdomen should be increased in a stepwise fashion and need not exceed 10–12 mmhg until hemodynamic stability is assured [16]. Rapid escalation or high insufflation pressures can impede preload and affect flow. LVAD monitoring equipment such as Near Infrared Spectroscopy (NIRS) and Doppler supplies should be present and properly functioning.

The patient's advance directives, such as goals for CPR, should be discussed during the pre op assessment. Two lines of thought arise with the need for cardiac compressions and whether it is safe for the LVAD device. On one spectrum, compressions should never be performed as components of the LVAD may be dislodged. On the other end, no incidences of this have ever been reported in a case study [3, 16]. It is a consensus of many that early defibrillation and optimization of LVAD dynamics should be the preferred method to achieve return of spontaneous circulation (ROSC). It is not uncommon for patients who are in ventricular fibrillation to be conversant and alert.

#### **4.2 Intraoperative phase**

Upon entering the OR, it is prudent to connect the drivetrain to wall power using a red outlet (one that would still work with emergency power) [16]. Do keep extra batteries available in case of power failure [26]. The battery life of HM3 is 10–12 hours. When plugged into wall power the monitor is large enough to display all VAD parameters at once [12]. It is very important to remind the staff that the LVAD will be plugged into the wall and to not unplug it or trip over the cord.

When applying standard vital sign monitors, be aware that traditional NIBP may not be obtainable because of the lack of pulsatile blood flow [16]. The pulse oximeter may periodically work due to intermittent pulsatility. In lieu of standard pulse oximetry, NIRS could be used to monitor cerebral blood oxygen content. Cerebral oximeters work by trending venous weighted oxyhemoglobin saturation [26].

Blood pressure and mean arterial pressure (MAP) can be monitored by an arterial line or Doppler device [3, 4, 8, 11, 16, 25]. Arterial lines are the gold standard for an LVAD patient undergoing general anesthesia [16, 19]. The waveform will have a somewhat flat appearance related to low pulse pressure [3]. The use of Doppler devices for blood pressure monitoring are recommended for smaller cases that involve local anesthesia or IV sedation/MAC. It is often necessary to have a dedicated person to measure this as it is a relatively time intensive process. In many institutions, an LVAD nurse accompanies the patient and is charged with this task. The technique uses a Doppler ultrasound at the brachial artery. The cuff is placed on the upper arm and inflated until loss of pulse. The cuff is then slowly deflated and the pressure at the return of signal noted. If the patient has a palpable pulse, the Doppler pressure is associated with systolic pressure. In the absence of a palpable pulse the noted

*Anesthesia for Non-Cardiac Surgery for the LVAD Patient DOI: http://dx.doi.org/10.5772/intechopen.111491*

pressure is associated with the mean arterial pressure [19, 25]. The Doppler pressure has been shown to correlate with arterial lines 88% of the time [14]. MAPs should be kept around 70–80 mmHg to prevent pump malfunction while ensuring end organ perfusion [4, 8, 11, 14, 16, 19, 20, 25, 26, 31]. Slow cuff method is another effective technique, but it is not widely available [16, 19]. The slow cuff system deflates more slowly than common non-invasive blood pressure devices (**Figure 10**) [19].

#### **4.3 Induction, maintenance, and emergence phases of anesthesia**

Almost any method of induction can be chosen provided hemodynamic purtubations are anticipated. Propofol induction, for example, is not contraindicated but conservative doses are less likely to cause significant hemodynamic swings. An inhalational induction, total, or in part, is also an option.

Using midazolam and ketamine can decrease the amount of other anesthetics. Opioids can decrease sympathetic tone and should be given judiciously. This author uses a balanced technique incorporating small titrated doses of midazolam, ketamine, and propofol to achieve unconsciousness using the minimum dose required. Often, a pre induction fluid bolus is given and a phenylephrine infusion is titrated to the desired mean arterial blood pressure.

Intubation and ventilation can potentially cause changes to VAD function. Airway manipulation can cause sympathetic stimulation and hemodynamic shifts. Although some sources say placement of a double lumen tube should be avoided in favor of a bronchial blocker for thoracic procedures, both have been placed successfully [20]. Positive pressure ventilation and PEEP can affect preload, as can hypercarbia, hypoxia, and acidosis [16, 20]. Valsalva maneuvers may also impede venous return [20, 24].

Generally, the axial flow of an LVAD depends exquisitely on preload and afterload. It pumps the delivered volume and ejects it systemically. The main objectives are therefore to avoid decreased preload, maintenance of afterload, and avoid

#### **Figure 10.**

*A flow diagram highlighting key points to consider when managing an LVAD patient in the operating room.*

inflow cannula obstruction. Although literature may state to maintain MAPs around 70-80 mmHg to ensure preload and pump function, it is important to pay particularattention to the patient's starting hemodynamics and use them as a target throughout the procedure. Studies have shown that a MAP less than 70 mmHg for greater than 20 minutes is "strongly associated with" acute kidney injury [26]. Avoiding hypovolemia cannot be stressed enough. Often, to optimize preload prior to induction, a judicious amount of fluid is given, and may include 1–2 bottles of 5% albumin [pisanksy]. One must be mindful of blood loss and insensible fluid losses. Arterial blood gas sampling and monitoring of the hematocrit is important. A more liberal transfusion target may be appropriate given ongoing losses. It is important to use irradiated and leukoreduced blood products as many of these patients will be transplant candidates.

It is also important to use inotropes in addition to vasopressors to maintain right heart function in presence of hypotension, particularly if known right heart dysfunction is already present. Chronic LVAD support changes RV geometry and RV dysfunction might exist but not be clinically apparent. Causes of RV failure intro can be due to multiple factors including the inflammatory cascade, blood product administration, hypoxia, hypercarbia, and acidosis, among many. Vasopressin is cited as a pressor of choice related to its lack of effect on the pulmonary vasculature [20, 28]. Milrinone infusion may also be employed to ensure decreased stress on the right ventricle [3, 11]. Lastly, a TEE machine and appropriately trained personnel can provide additional insights if management is difficult or intraoperative adventures are encountered.

### **4.4 Positioning**

Positioning of the patient with an LVAD requires much attention for multiple reasons. For one, patient positioning can affect a patient's preload, pressure or impingement on the drivetrain, and/or access to the patient to obtain Doppler pressures [11, 20]. Positions such as beach chair, reverse Trendelenburg, prone, and lateral will all decrease preload, and hence, impair proper functioning to the LVAD. As some surgical procedures may necessitate these undesirable positions, a discussion involving potential alternatives with the surgeon or slowly advancing the patient to the desired position as hemodynamically tolerated is imperative [16]. Prone positioning and any position that could affect the positioning of the inflow cannula should be readily reversible. Vigilant attention should also be paid to the driveline cable as it exits the patient typically from the upper abdomen and is the power source to the LVAD. When positioning care should be taken to make sure the cable is not pulled, kinked, or applying excessive pressure to the patient's skin [16].

## **4.5 Troubleshooting hemodynamic changes with LVAD patients under anesthesia**

**Figure 11** lists some acute complications that might occur perioperatively while the patient is under anesthesia and some immediate actions to take. Acute hypertension could be caused by sympathetic response to intubation or to surgical stimulation. MAPs above 90 mmHg can affect pump function and should be immediately treated by increasing anesthetic depth or titrating small increments of antihypertensives. Currently there is no standardized management of hypertension in LVAD patients [14]. If hypertension should arise and forward LVAD flow becomes impeded, anesthetic depth can be titrated [18]. Hydralazine is noted to be an appropriate and

#### **Figure 11.**

*Intra operative troubleshooting of an LVAD patient under general anesthesia.*

effective choice to treat HTN in LVAD patients. Beta blockers are cautioned because of their negative inotropic effect [4, 11].

Suck down phenomenon can occur with decreased left ventricular filling. The VAD will suction onto the septal wall with low volumes [3, 4, 16]. Suction event may be recognized by speed, flow, and power values all being decreased [3] or low left ventricular volumes on the transesophageal echocardiogram [3, 16]. Treatment for suction events is to slow the VAD speed to allow increased filling of the ventricle, support with vasopressin, and increase preload via fluid bolus [4, 16]. Suction events may trigger ventricular tachycardia.

If an LVAD patient presents with ventricular tachycardia (VT), one should consider placing R2 pads prior to induction. R2 pad placement is the same as for non-LVAD patients and shocking with R2 pads does not disrupt LVAD function. Suction events are the most common cause of VT in LVAD supported patients [4, 16]. It is possible that some patients will be hemodynamically stable during episodes of VT as LVAD will continue to function. Additional treatment for VT includes 300 mg IV boluses of amiodarone [11]. A hemodynamically unstable patient may require advanced cardiac life support measures [3].

Post induction hypotension is best prevented by slow thoughtful induction, as described earlier. In the event of hypotension placing the patient in slight Trendelenburg and decreasing positive pressure ventilation, for positive pressure ventilation can put strain on the RV and decrease preload [16]. Small fluid bolus and titration of vasopressors should be used to support blood pressure and maintain preload.

Pump malfunction alarms may indicate the pump is not functioning, power is disrupted, or flow rate has changed. Consult the LVAD specialist. Meanwhile check that all connections are intact, from the wall/battery to the control panel to the driveline. Check the driveline for connections, kinks, or damage. If an alarm is sounding because of low or high flow rates use the diagrams in **Figures 7** and **8** to recognize a pattern of changes and identify a potential cause.

## **4.6 Post-operative**

Patients can be recovered in PACU but may be recovered in the ICU [11, 16, 20]. The AICD should be interrogated as soon as possible in the immediate postoperative period. It is paramount to take steps to prevent increased preload by way of hypoventilation and hypertension related to pain [16]. Opioid sparing techniques are suggested for pain control to prevent hypoventilation and sequela post operatively [16, 20]. Again, the focus is to maintain pump flow and pre-operative physiology [18]. Post operative readmissions to the hospital are common as patients with LVADs undergoing non cardiac surgery have high rates of bleeding and acute kidney injury. The need for transfusion may be delayed several hours post surgery [7].

## **4.7 Case studies for LVAD patients and non cardiac surgery**

A. A 24-year-old parturient with a heartware HVAD requests an epidural placement for induction of labor and subsequent cesarean section. The patient stopped lovenox 24 hours prior to hospital admission.

Once admitted, invasive BP monitoring, central line and Swan Ganz placement were performed.

Subsequently, an epidural catheter was placed prior to induction of labor. The patient was permitted a patient-controlled epidural device (PCEA) that dispensed a bupivacaine and fentanyl solution. With the decision to perform cesarean section the epidural was dosed with 2% lidocaine in small increments. Vasopressin and norepinephrine drips were used throughout to maintain MAPs greater than 70 mmHg.

The patient received transverse abdominal plane blocks post operatively for pain control. No complications with the LVAD were noted [28].


D. A 66-year old male with a HMII with prostate cancer present for robotic laparoscopic prostatectomy.

Prior to the surgical date the patient had a ramp transthoracic echocardiogram to optimize his LVAD function. The patient was admitted the night prior to his procedure for LVAD and ICD interrogation. His warfarin was held the night before surgery. An INR of 3.2 was noted prior to surgical start time, prothrombin complex concentrate was administered; prior to incision INR was 1.4. An arterial line and right internal jugular central venous catheter were placed prior to induction. A rapid sequence induction was performed with 1.5 mcg/kg fentanyl, 1 mg/kg of propofol, and 1.2 mg/kg rocuronium. Anesthesia was maintained with sevoflurane. Post induction the patient became hypotensive and was treated with a 250 mL bolus of albumin. With the start of pneumoperitoneum the patient became hypertensive. This was managed with a bolus of propofol and initiation of dobutamine and nicardipine drips to maintain preload and afterload. As the patient was transitioned into trendelenberg a rise in central venous pressure was noted, but LVAD parameters maintained within the patient's normal range and no action was taken at that time. Approximately 40 minutes after being positioned in trendelenberg the CVP had increased significantly and the PI was decreasing. A cardiac anesthesiologist was consulted for TEE, which showed septal bowing and right ventricular dysfunction. Inhaled epoprostenol was administered as treatment, CVP and PI returned to baseline. During desufflation of the pneumoperitoneum the patient became hypotensive requiring a second albumin bolus and short term epinephrine and phenylephrine drips while the surgical procedure finished. All drips were weaned off; the patient was extubated and taken to the cardiac intermediate care unit to recover. No postoperative complications were noted and the patient was discharged to home 2 days postoperatively [33].

## **5. Discussion**

It is estimated that by 2030, the number of Americans with heart failure will increase to over 8 million [1, 5]. The number of heart transplants per year has been between 2 and 5 thousand and will continue to be limited by the number of donors. Donor availability may soon increase related to hepatitis C no longer disqualifying donation, however, even this breakthrough is not anticipated to fulfill the need for heart transplant patients [5, 23]. Therefore, there is likely to be an increased need for alternative definitive treatment for advanced heart failure, such as LVADs.

There is a campaign to recognize advanced heart failure sooner and to implant an LVAD before patients develop significant end organ disease [4, 23]. The strategy is to standardize criteria across all LVAD centers. One suggestion is to use AI algorithms to evaluate electronic medical records for increased frequency of visits and other criteria indicative of advancing heart failure [23].

Current targets for advancement include development of a completely implantable device and standardization of minimally invasive surgery (MIS) technique for LVAD implantation [23]. MIS technique requires two thoracotomy incisions; one 2 centimeters at the right intercostal space and a second larger (8-10 cm) at the 5-6th intercostal space. These incisions expose the ascending aortic arch and apex of the left ventricle, respectively [34]. In addition to preserving the sternum MIS affords less blood loss, less need for transfusion, and less intrathoracic trauma [22, 23, 34]. One retrospective study

also noted patients who underwent MIS placement had significantly shorter time to extubation, less incidence of RV failure, shorter ICU time, and fewer readmissions [34].

The fully implantable device has the potential to significantly decrease incidence of LVAD infections [4]. Three fully implantable devices have been developed and begun trials. The Abicor total artificial heart and the Arrow Lion heart did not achieve long term survival but showed significantly lower infection rates than devices with extracorporeal components [23].

A 2019 paper reported two patients received Jarvik 2000 LVADs designed without any percutaneous parts. The modified devices were produced to trial with a coplanar power system. The coplanar energy transfer system (CETS) wirelessly transfers energy from an external energy source to the internal battery/controller component, which directly powers the LVAD. When fully charged the internal battery system provides up to 6 hours of power. The system also includes a wristwatch monitor to display parameters. Patient A was noted to have an intraoperative neurological complication but pump implantation was successful. This patient developed a pump thrombus, in conjunction with his complicated postoperative course the device was turned off and the patient maintained on inotropes.

Patient B had a successful implantation and was discharged 30 post implantation. No infections or issues with the CETS were noted during either patients' hospital stays. No long term follow up information was available at the time of this publication [35].

A fourth device, the Calon Leviticus fiVAD is under development in Europe. In a preclinical study the fully implantable device completed a promising 6 day trial in sheep. It was paired with the same coplanar power system as the Jarvik trial mentioned above [36].

The technology of the LVAD has improved drastically over the last two to three decades increasing the longevity of these devices and those who benefit from them. Currently 1 year survival is 90% and mid 80% for heart transplant and LVAD respectively [4]. As these devices continue to improve and the common complications are better understood and managed, LVADs have the potential to become the preferred treatment for severe heart failure [4].

## **6. Conclusion**

The LVAD was originally intended to support the patient with heart failure until a donor heart became available. Today they are implanted for a variety of therapeutic intentions and have extended the life span of critical heart failure patients. LVAD implantation changes the physiology of the heart and comes with some related complications. Caring for this patient population takes extra planning, optimization, and coordination. Adjustments to pre op assessment, monitoring devices, and peri operative management will be needed. However, by understanding these devices and related physiological changes, a non-cardiac anesthesia provider can safely administer a variety of anesthetics to a patient with an LVAD presenting for non-cardiac surgery.

## **Conflict of interest**

The authors declare no conflict of interest.

*Anesthesia for Non-Cardiac Surgery for the LVAD Patient DOI: http://dx.doi.org/10.5772/intechopen.111491*

## **Author details**

Kathryn Foster\* and Steven S. Silvonek Department of Anesthesiology, St. Luke's University Health Network, USA

\*Address all correspondence to: kafoster1223@gmail.com

© 2023 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Section 4
