Out-of-Operating Room Procedures—Adult

Charles DeBattista MD (Electroconvulsive therapy)

L. Bing Liem DO (DC cardioversion, ICD)

Michael P. Marks MD (Interventional neuroradiology)

Stephen T. Kee MD (Tracheobronchial stenting, RFA, IRE)

Daniel Y. Sze MD, PhD (Image-guided procedures)

Joan K. Frisoli MD, PhD

Eric J. Sirulnick MD

John Brock-Utne MD, PhD

Richard A. Jaffe MD, PhD

PROCEDURAL SPECIALISTS

ANESTHESIA FOR OUT-OF-OPERATING ROOM PROCEDURES

GENERAL COMMENTS

Advances in the fields of radiology, cardiology, and neurology have led to an increase in the number of anesthesia procedures performed away from the OR. In line with these changes, the ASA has provided guidelines for the safe delivery of anesthesia at locations remote from the OR environment.

Anesthetic considerations for out-of-OR locations (modified from ASA Guidelines¹) include

Primary and backup O₂ sources (e.g., piped O₂ + 1 full E cylinder)
Adequate and reliable suction
Adequate and reliable scavenging system (for inhalational anesthesia)
Self-inflating hand resuscitator bag with ability to deliver at least 90% O₂
Adequate anesthetic drug supplies and equipment
Adequate monitoring equipment to allow adherence to the “Standards of Basic Anesthetic Monitoring”²
Sufficient electrical outlets connected to an emergency power supply
Wet locations (e.g., cysto, arthroscopy, labor, and delivery) should be equipped with either an isolated electrical source or circuits with ground-fault interrupters.
Adequate illumination for patient observation and monitoring equipment (flashlight backup)
Sufficient space for expeditious access to patient, machine, and support equipment
Emergency cart with defibrillator immediately available
Immediate access to skilled anesthesia support personnel

Suggested Readings

1. American Society of Anesthesiologists: Guidelines for Non-Operating Room Anesthetizing Locations. American Society of Anesthesiologists, Park Ridge: 2008.

2. American Society of Anesthesiologists: Standards for Basic Anesthetic Monitoring. American Society of Anesthesiologists, Park Ridge: 2011.

3. Eichhorn V, Henzler D, Murphy MF: Standardizing care and monitoring for anesthesia or procedural sedation delivered outside the operating room. Curr Opin Anaesthesiol 2010; 23(4):494-9.

4. Metzner J, Domino KB: Risks of anesthesia or sedation outside the operating room: the role of the anesthesia care provider. Curr Opin Anaesthesiol 2010; 23(4):523-31.

ELECTROCONVULSIVE THERAPY (ECT)

PROCEDURAL CONSIDERATIONS

Description: Electroconvulsive therapy (ECT) is the transcutaneous application of small electrical stimuli to the brain to produce generalized seizures for the treatment of selected psychiatric disorders, such as severe depression. There are several important aspects of ECT that are of relevance to the anesthesiologist. The first is the uncontrolled motor activity associated with generalized seizures. Prior to introduction of GA, the most common injuries associated with ECT were compression fractures of the vertebral bodies and broken limbs from violent tonic-clonic motor activity. Even with complete paralysis, the masseter muscles are directly stimulated to contract during seizure induction. As a result, the most common injury currently associated with ECT is broken teeth.

A second consequence of ECT induction is that the electrical stimulus can cause contraction of cranial musculature and a brief dilation of meningeal blood vessels, resulting in postictal headaches in up to 40% of patients. Patients < 50 yr and those with a Hx of migraine headaches appear most at risk for post-ECT headaches that may occasionally require aggressive pain management. Finally, ECT may be a significant hemodynamic stressor. Initially, central parasympathetic centers are activated, resulting in bradydysrhythmias in ˜30% of patients. Brief sinus pauses are not uncommon. The initial parasympathetic effects are followed by sympathetically mediated increases in HR and BP up
to 20-30% above baseline. Mean arterial blood pressure has been known to double in some instances. These cardiovascular responses can persist for minutes to an hour or more after the procedure is completed.

The optimal position for ECT is supine. Occasionally, the head is kept slightly raised to help maintain an adequate airway and decrease anxiety. Patients typically come to ECT quite anxious about the procedure. ECT is generally performed in a PACU or specialized ECT suite. In many centers, outpatients make up the majority of patients seen for ECT. The electrical stimulus is applied through plastic adhesive leads prepared with a contact gel. These leads are usually applied to the forehead in a bitemporal or right unilateral placement. Monitoring typically includes a twolead electroencephalogram (EEG) and frequently an electromyogram (EMG) to measure motor activity. A BP cuff is inflated to act as a tourniquet and prevent neuromuscular blockade in the distal limb. Thus, an arm or leg can be used to measure motor duration of the seizure. A special ECT device is used to generate the appropriate electrical stimulus. Seizures are typically 30-90 sec in duration, and the entire procedure—from the induction of anesthesia to patient awakening—is generally < 15 min. The recovery period averages 45-90 min and allows for monitoring of vital signs, as well as the opportunity for the postictal confusion to clear. Patients can wake up mildly confused-to-frankly delirious and require close nursing supervision. Postictal agitation is also quite common and may require an intervention. Treatments are typically performed every other day, and the average number of treatments is 6-12 in the acute management of major depression. However, ECT treatments currently tend to be tapered rather than stopped abruptly. Thus, the frequency of treatments may go from 3/wk for acute treatment, to 1/wk, 2/mo, and finally 1/mo. Maintenance ECT with a frequency ranging from every few weeks to every few months is commonly prescribed for those patients who respond to ECT but fail to benefit from pharmacotherapy.

The most common morbidities associated with ECT include headaches and myalgias. Postictal confusion is the rule, and some anterograde and retrograde memory loss occurs in most patients who have completed an acute course of ECT. Memory loss is typically confined to the period immediately before, during, and immediately after an acute series of ECT. There tends to be a cumulative memory loss with subsequent ECT treatments within a given series. In most patients, memory deficits largely subside in the first 1-3 mo following an acute series of treatments. In rare instances, autobiographical memory loss has been reported for months or years after an ECT series has been completed. Long-term memory loss appears to be more common with bilateral lead placement. In addition, ECT-related mortality is estimated at approximately 4/10,000. Cardiac events account for 67% of all ECT-related deaths, with malignant arrhythmias and MIs accounting for most fatalities. Pulmonary events (obstruction, pulmonary edema, or emboli) account for most additional mortality. Cerebrovascular infarctions or hemorrhages have rarely been reported with ECT.

Usual preop diagnosis: Depression; mania; catatonia; refractory psychosis

▪ SUMMARY OF PROCEDURE

Position	Supine
Incision	None
Special instrumentation	Seizure generator & electrodes; EEG/EMG monitors
Unique considerations	Requires muscle relaxation to prevent injury. 50-80 mg of succinylcholine is usually sufficient. Using larger dose of succinylcholine can lead to patient waking up while paralyzed. Nondisposable bite blocks are required to prevent dental injury. Apply tourniquet (BP cuff) to one arm before administration of muscle relaxant. A slow heart rate preop may require atropine. A high BP preop may require aggressive hypotensive Rx with beta-blockers, phentolamine, hydralazine, etc. If the seizure duration is not > 25 sec, then another seizure may be ordered. Give more induction agents as needed. Because one arm is not paralyzed, asking the patient to squeeze your fingers will tell you that she/he is awake.
Antibiotics	None
Procedure time	Setup: 5-10 min Treatment: < 10 min (seizure duration 25-280 sec)
Postop care	PACU → room or home
Mortality	4/10,000
Morbidity	HA/myalgias/nausea: Common Confusion/memory loss: Common. Be aware that postoperative hypoxia can present with confusion. Cardiac dysrhythmias: 10-40% (brief asystole common). Keep a close eye on the EKG. MI: Rare Pulmonary edema from excessive iv fluids: NOT uncommon. Pulmonary aspiration and/or negative pressure pulmonary edema: Rare CVA: Rare
Pain score	2-3 (HA)

▪ PATIENT POPULATION CHARACTERISTICS

Age range	≥ 18 yr. ECT is rarely performed in adolescents and preadolescents; however, patients in their 90s are sometimes candidates for ECT. There is a preponderance of geriatric patients on many ECT services.
Male:Female	1:2
Incidence	The lifetime prevalence of major depression (the primary indication for ECT) is ˜17%; 26% of women and 12% of men are affected. < 1% of patients with major depression undergo ECT, and approximately 400,000 ECT procedures are performed in North America annually.
Associated conditions	Substance abuse (30% of all depressed patients meet criteria for alcohol or drug abuse); panic attacks (30% of depressed patients); psychotic symptoms (14% of patients); HTN and sinus tachycardia; dehydration; self-inflicted trauma; pregnancy.

ANESTHETIC CONSIDERATIONS

PREOPERATIVE

Patients presenting for ECT usually have failed to respond to antidepressants; however, most will continue to take psychotherapeutic agents. Many of the older patients will be taking other medications for coexisting medical conditions. Drug interactions are an important consideration for the anesthesiologist (see Drug Interactions, p. F-1). The most commonly used medications are listed in Table 13.1-1.

Anesthesia for ECT may seem to be a benign procedure; however, these cases—which seldom take > 20 min— can prove very challenging, especially in the geriatric population. ECT can place significant stress on the cardiovascular system; therefore, particular care should be taken to evaluate and optimize the patient’s pretreatment cardiovascular status. ECT usually takes place in remote locations, so the anesthesiologist must ensure that the location is properly equipped and complies with ASA Guidelines for Out-of-OR Procedures (see p. 1484) and Standards for Basic Anesthetic Monitoring.

Table 13.1-1. Commonly Used Medications in the Treatment of Depression

Tricyclic	MAOI	SSRI	SNRI and Other Antidepressants
Amitriptyline (Elavil, others) Amoxapine (Asendin) Desipramine (Norpramin) Doxepin (Sinequan) Imipramine (Tofranil) Maprotiline (Ludiomil) Nortriptyline (Pamelor) Protriptyline (Vivactil) Trimipramine (Surmontil)	Isocarboxazid (Marplan) Phenelzine (Nardil) Tranylcypromine (Parnate) Transdermal selegiline (Emsam) Lithium (Often used as an adjunctive agent/mood stabilizer in depression)	Fluoxetine (Prozac) Paroxetine (Paxil) Sertraline (Zoloft) Fluvoxamine (Luvox) Citalopram (Celexa) Escitalopram (Lexapro)	Venlafaxine (Effexor) Duloxetine (Cymbalta) Nefazodone (Serzone) Mirtazapine (Remeron) Bupropion (Wellbutrin) Trazodone (Desyrel) Atypical Antipsychotics (Used adjunctively) Olanzapine (Zyprexa) Quetiapine (Seroquel) Aripiprazole (Abilify) Risperidone (Risperdal) Ziprasidone (Geodon)
MAOI = Monoamine oxidase inhibitor
SSRI = Selective serotonin reuptake inhibitor
SNRI = Selective norepinephrine/serotonin reuptake inhibitor

Respiratory	These patients will require airway management and PPV. Hence, preop assessment of the airway must focus on the ease of mask ventilation and the potential need for ET intubation (e.g., airway compromise or severe GERD).
Cardiovascular	A recent MI (< 3 mo) is a contraindication to ECT. Relative contraindications include aortic aneurysm, angina, CHF, and thrombophlebitis. The presence of dysrhythmias, a pacemaker, or ICD is not a contraindication for ECT. For the patient with a pacemaker, a means (e.g., a magnet) should be available to convert the pacemaker to an asynchronous mode. Patients on long-term anticoagulation therapy may require pre-ECT dose adjustment (target INR 1.5-2.5) or they should switch to heparin before each ECT session and return to their standard therapy post-ECT. Tests: As indicated from H&P
Gastrointestinal	Patient should be npo. Patients with Sx of GERD should be pretreated with Na citrate (30 mL po), ranitidine (50 mg iv), and metoclopramide (10 mg iv). ET intubation should be considered for all patients at risk for aspiration.
Neurological	ECT is relatively contraindicated in the presence of ↑ ICP, and recent CVA (< 3 mo), intracranial mass lesions, or recent intracranial surgery (< 3 mo).
Endocrine	Presence of a pheochromocytoma (Sx of which may be confused with a psychiatric disorder) is a contraindication to ECT. < 1% of hypertensive patients will have a pheochromocytoma.
Genetic	[check mark] for family Hx of pseudocholinesterase deficiency. Mivacurium (0.15 mg/kg) is a suitable alternative to succinylcholine. Tests: Dibucaine number (normal ≥ 80) and serum cholinesterase level, if indicated from H&P.
Hepatic	Hepatotoxicity has been associated with use of MAOI. Tests: Consider LFTs for patients on chronic MAOI therapy.
Orthopaedic	In patients susceptible to bone fracture (e.g., severe osteoporosis, osteoporosis imperfecta), an increased succinylcholine dosage (1.5 mg/kg) is given to ensure profound muscle relaxation. Patients with severe rheumatoid arthritis may have unstable C-spine, and extreme care should be taken during positioning of head and neck.
Ophthalmologic	Retinal detachment is a relative contraindication to ECT. Succinylcholine should be avoided in patients with glaucoma treated with cholinesterase-inhibitors (e.g., echothiophate). Mivacurium (0.15 mg/kg) is a suitable alternative.
Pregnancy	Pregnancy is not a contraindication for ECT (even in the third trimester). After the 4th mo, the need for full-stomach precautions requires rapid-sequence induction and ET intubation (see p. B-5). Left uterine displacement should be maintained during treatment. Monitor fetal heartbeat.
Psychiatric drugs	Patients receiving tricyclic antidepressants (TCAs) may have an exaggerated pressor response to direct-acting sympathomimetic drugs, with the potential for tachycardia, dysrhythmias, and hyperthermia. The response to indirect-acting sympathomimetic drugs (e.g., ephedrine) may be attenuated in these patients. TCAs also will increase the effects of anticholinergic drugs (e.g., glycopyrrolate, atropine). Patients receiving MAOIs will exhibit exaggerated responses to indirect-acting sympathomimetic drugs (e.g., ephedrine). In addition, in these patients, succinylcholine metabolism is inhibited (↑ NMB), and meperidine is contraindicated (↑↑ BP, ↑ Sz, ↑↑ T). It is probably unnecessary to discontinue TCAs or MAOIs prior to ECT, as long as these interactions can be avoided. Lithium should be discontinued for at least 3 d prior to ECT to avoid delayed recovery and subsequent posttreatment agitation and confusion. Lithium also is associated with ↑ NMB (succinylcholine and pancuronium). SSRIs have been associated with prolonged ECT-induced seizure duration and adverse behavioral/neurological effects following haloperidol administration (use droperidol and metoclopramide with caution). No adverse interactions have been reported between anesthetic agents and SSRIs or SNRIs.
Laboratory	Tests as indicated from H&P
Premedication	Although usually not required, some patients may benefit from an antisialagogue (glycopyrrolate 0.2 mg iv). Patients with Hx of postop N/V will benefit from a prophylactic antiemetic (e.g., ondansetron 4 mg iv). Patients with postseizure muscle pain and headache may benefit from ketorolac (30 mg iv). Some patients will require 500-1,000 mg caffeine iv, or po, to decrease seizure threshold. The iv caffeine effect should be manifest in 5 min. However, po caffeine must be given 30-40 min in advance. Verapamil (not adenosine, which is blocked by caffeine) should be available to control supraventricular tachycardia (0.07-0.25 mg/kg over 2 min). Labetalol, hydralazine, esmolol, and diltiazem are alternative drugs for control of HR and BP.

INTRAOPERATIVE

Anesthetic technique: A review of previous anesthetic records is very helpful in formulating the anesthetic plan and in anticipating physiological changes unique to each patient. Usually brief iv anesthesia (mask oxygenation and ventilation) with muscle relaxation (1-2 twitches) is required to prevent patient injury during seizures. Prior to induction, a tourniquet (BP cuff) is applied to the non-iv arm and inflated to a pressure above systolic. This prevents neuromuscular blockade distal to the cuff and permits direct monitoring of seizure activity. Preop BP control (e.g., labetalol 5-20 mg, diltiazem 10-20 mg iv, or esmolol 0.5-1 mg/kg iv in increments) is often necessary.

Induction	Preoxygenation should be attempted in all patients. In some patients who are intolerant of a mask, a less-intrusive blow-by technique may be tried. Anesthesia is induced with propofol (1-2 mg/kg), sodium methohexital (0.5-1 mg/kg), or etomidate (0.1-0.2 mg/kg). An induction dose of etomidate will block stress-induced cortisol production for up to 24 h. Propofol (1-1.5 mg/kg) may be used, but may shorten seizure duration. TCAs and MAOIs can increase sleep time. After tourniquet inflation, succinylcholine (0.8-1 mg/kg) is injected to induce paralysis. Hyperventilation is carried out to enhance seizure activity. A bite block is placed, and then the patient is ready for ECT. In barbiturate-tolerant patients, remifentanil (1-3 mcg/kg) has been used as a means of reducing the barbiturate dose, thereby permitting adequate seizure duration. Patients receiving remifentanil need minimal postseizure BP control.
Maintenance	Given the brevity of this procedure, maintenance of anesthesia is rarely a concern; however, occasionally a second or third treatment may be necessary if the seizures are of inadequate duration (< 25 sec) and quality. In this case, a subsequent dose (10-30 mg) of succinylcholine may be needed. Assisted ventilation is necessary until spontaneous ventilation resumes. Of major concern during the seizure period is the hypertensive response. Some patients may need to be treated prior to induction of anesthesia with either labetalol (5-20 mg iv) or esmolol (10 mg q 1 min) to control HR/BP. SNP (5-50 mcg/bolus iv) is useful to control BP in refractory cases. Profound ↓ HR may occur in the immediate post-ECT period requiring atropine or a chest thump.
Emergence	Patients should be awake within 5-10 min postseizure and often are disoriented. Small doses of midazolam (e.g., 0.25-0.5 mg iv) may help to control agitation, and blow-by O₂ may be less stimulating. ASA guidelines for postanesthesia care should be followed (see p. 1484).
Blood and fluid requirements	No blood loss IV: 20 ga × 1 NS/LR @ TKO
Monitoring	Standard monitors (see p. B-1) Tourniquet EEG EMG	Seizure activity is usually monitored by a psychiatrist observing the tourniqueted limb and by measuring EMG and EEG activity. (These monitors are usually an integral part of the ECT seizure generator.)
Positioning	Supine
Complications	Dysrhythmias Tachydysrhythmias ↑ BP Dental damage Pulmonary edema Aspiration	Brief periods of asystole and profound bradycardia are not uncommon (usually related to parasympathetic overactivity). Treatment is rarely necessary. Responds well to esmolol (10-15 mg iv) or lidocaine (1 mg/kg iv), although treatment is usually unnecessary. ↑ BP readily responds to esmolol (10-30 mg) or labetalol (5-20 mg). In refractory cases, 10-50 mcg of SNP may be necessary. Use of bite block is essential. Dental damage is not prevented by muscle relaxation (direct electrical stimulation of facial and jaw muscles).

POSTOPERATIVE

Complications

HA, myalgias

N/V

Disorientation

Memory impairment

MI/ischemia

Dysrhythmias

Pulmonary edema/aspiration

↑ BP

Rx: ketorolac 30 mg iv

Rx: ondansetron 4 mg iv

Rx: midazolam 0.25-0.5 mg iv

Prolonged ↑ BP is unusual and may suggest the need for further workup.

Suggested Readings

1. Allan CL, Ebmeier KP: The use of ECT and MST in treating depression. Int Rev Psychiatry 2011; 23(5):400-12.

2. Cohran M, DeBattista C, Schmiesing C, et al: Negative pressure pulmonary edema. A potential hazard in patients undergoing ECT. J ECT 1999; 15:168-70.

3. DeBattista C, Cohran M, Barry JJ, et al: Fetal heart deceleration during ECT induced seizures: is it important? Acta Anaesth Scand 2003; 47:101-3.

4. Deiner S, Frost EA: Electroconvulsive therapy and anesthesia. Int Anesthesiol Clin 2009; 47(2):81-92.

5. Kurup V, Ostroff R: When cardiac patients need ECT—challenges for the anesthesiologist. Int Anesthesiol Clin 2012; 50(2):128-40.

6. MacPherson RD, Loo CK: Cognitive impairment following electroconvulsive therapy- does the choice of anesthetic agent make a difference? J ECT 2008; 24(1):52-6.

7. Mirzakhani H, Welch CA, Eikermann M, Nozari A: Neuromuscular blocking agents for electroconvulsive therapy: a systematic review. Acta Anaesthesiol Scand 2012; 56(1):3-16.

8. Sharp RP, Welch EB: Takotsubo cardiomyopathy as a complication of electroconvulsive therapy. Ann Pharmacother 2011; 45(12):1559-65.

9. Smith D, Angst M, Brock-Utne JG, et al: Seizure duration with remifentanil/methohexital vs. methohexital in middle aged patients undergoing ECT. Acta Anaesth Scand 2003; 47:1064-6.

INTERVENTIONAL NEURORADIOLOGY

PROCEDURAL CONSIDERATIONS

The indications for endovascular therapy for the brain and spine have continued to grow with the technical strides made in both devices and imaging. Endovascular therapy is now widely used in the treatment of intracranial aneurysms, arteriovenous malformations (AVMs), arteriovenous fistulas (AVFs), and tumors. It also is extensively used in revascularization of the cerebral circulation in the setting of acute stroke or for the treatment of cerebrovascular stenoses. Many of these procedures can be performed with the patient awake; however, GA or deep sedation often is used to minimize patient movement during procedures that require careful catheter and device control for safe operation. These procedures can be divided into three broad categories: (a) embolization, (b) aneurysm therapy, and (c) cerebral revascularization.

EMBOLIZATION

This therapy may be used for a variety of lesions, including AVMs in the brain; dural AVFs; vein of Galen malformations; vascular neoplasms, such as meningiomas, hemangiomas, glomus tumors, and juvenile nasal angiofibromas; and for treatment of epistaxis.

AVM embolization usually is performed as an adjunct to radiosurgery or microsurgery, although in selected cases, embolization may be the definitive treatment. Brain AVMs are generally parenchymal lesions with multiple feeding pial arteries and draining veins. The goal of embolization is to reduce the size and shunt burden presented by the AVM before either radiosurgery or microsurgical resection. Liquid embolic agents are preferred, with n-butyl cyanoacrylate (NBCA) and ethylene vinyl alcohol copolymer (EVOH) being the two materials currently used for the procedure. Embolization often is preceded by neurophysiologic testing, which may include the superselective injection of a barbiturate into the portion of the intracranial circulation being considered for embolization. Some centers perform the procedure with the patient awake to allow for more thorough clinical testing prior to embolization, while others prefer the patient to have general anesthesia to minimize patient motion.

Dural arteriovenous fistulas involve dural veins or sinuses and are most commonly located in the regions of the cavernous, transverse, and sigmoid sinuses. Because of their location, these malformations usually are supplied from meningeal arteries. A cavernous sinus fistula also may develop as a direct large-hole fistula between the internal carotid artery and the cavernous sinus. Patients may have a variety of symptoms depending on the location, size, and drainage pattern of the dural fistula. The embolization process for these dural-based lesions differs somewhat from the technique used for pial-based brain AVMs. Arterial embolization may be used, but venous embolization is often used to definitively occlude the fistula. Embolization of meningeal arteries may be preceded by clinical testing for cranial nerve deficits. This usually is accomplished with the superselective injection of lidocaine before embolization, and it is often preferred to have the patient awake for this procedure. If arterial embolization is utilized, a liquid embolic (NBCA or EVOH) is often utilized. Venous embolization is usually done with platinum coil occlusion.

Vein of Galen malformations are congenital lesions that may present in infancy or early childhood. Presenting symptoms include CHF, hydrocephalus, and neurodevelopmental delay. These lesions often require a staged approach to treatment and present a special challenge in the neonate or infant. In general, arterial embolization is performed as the initial endovascular approach, and a liquid embolic agent is used. In some cases, this may be augmented by a venous approach, with embolization using platinum coils.

Tumor embolization usually is performed as an adjunct to the surgical resection of highly vascular tumors (e.g., meningiomas, hemangiomas, hemangioblastomas, glomus tumors, and juvenile nasal angiofibromas). Generally, arterial embolization of meningeal supply vessels is done before surgery, using PVA or trisacryl gelatin microspheres. Physiologic testing with superselective injection of lidocaine often precedes embolization. When there is tumor encasement of a major artery, the patient may also undergo balloon test occlusion followed by permanent occlusion to reduce the risk of intraoperative bleeding.

ANEURYSM THERAPY

Endovascular therapy is the treatment of choice for many intracranial aneurysms, and it consists of either direct intraaneurysmal obliteration with detachable platinum coils or placement of a flow-diverting stent in the parent artery to produce thrombosis of the aneurysm. A randomized, controlled trial has shown better clinical outcome for patients treated with aneurysm coiling than surgical clipping in the setting of acute subarachnoid hemorrhage. Narrow-necked aneurysms are usually treated with a microcatheter through which coils are introduced directly into the aneurysm. Wider-necked aneurysms are more difficult to treat using this technique because coils may prolapse into the parent artery. In this situation, coiling may be done with either balloon remodeling or the combined use of a stent. Balloon remodeling involves placing a balloon catheter in the parent artery over the ostium of the aneurysm. The balloon is intermittently inflated with each coil insertion to prevent coil prolapse into the parent vessel. Fenestrated stents can also be introduced into the parent artery over the ostium of the aneurysm. The aneurysm is coiled by placing a microcatheter through the stent fenestrations into the aneurysm. Parent artery occlusion is still used for some giant or fusiform aneurysms, but has more recently been largely replaced by the use of flow-diverting stents (e.g., Pipeline™). Parent artery occlusion is generally done in a two-step process. Test occlusion is initially performed with a balloon-tipped catheter, and the patient is evaluated using clinical testing and neurophysiological monitoring. The testing may be done with controlled hypotension to improve the test sensitivity. If the patient
tolerates test occlusion, a permanent occlusion is usually done using coils placed into the parent artery. More recently, flow diverter stents have been used to treat giant and wide-necked aneurysms (see Fig. 13.1-1). These stents are constructed using fine mesh self-expanding metal. They are placed in the parent artery to reduce blood flow into the aneurysm sac resulting in gradual thrombosis of the aneurysm while maintaining flow in the parent artery. This treatment is generally reserved for unruptured aneurysms as the patients require treatment with antiplatelet agents.

Figure 13.1-1. Example of a fine mesh, flow-diverting stent (Pipeline™) used to treat a wide-neck aneurysm.

CEREBRAL REVASCULARIZATION

Acute stroke thrombolysis or thrombectomy is performed to recanalize larger occluded arteries in the cerebrovascular circulation, including the internal carotid, middle cerebral, vertebral, and basilar arteries. Intravenous tissue plasminogen activator (IV-tPA) is used up to 4.5 h following acute stroke onset. Intraarterial thrombolytics and thrombectomy devices are used when IV-tPA has failed to open the occluded artery or patients present beyond 4.5 h. Physiologic imaging with either CT or MR is used at many centers to select patients who will benefit from treatment in these more extended time windows. The FDA has recently approved a device for mechanical thrombectomy in the setting of stroke. These devices include a suction thrombectomy catheter, which can be introduced into the intracranial circulation, and retrievable stents, which are introduced into the thrombus and after entrapping the thrombus are pulled from the circulation. In addition, many endovascular therapists employ intraarterial thrombolytics either alone or combined with a mechanical thrombectomy device.

Angioplasty and stent placement for symptomatic atherosclerotic stenosis in the cerebrovascular circulation are becoming more widely performed in lieu of medical or direct surgical therapy. Stents with distal protection devices
have now been approved for the treatment of cervical carotid artery stenosis. Distal protection devices (e.g., balloon or basket devices) have been shown to reduce the thromboembolic complication rate and are now required for treatment in most cases. A recent large multicenter trial of both symptomatic and asymptomatic carotid stenosis patients found the composite risk of stroke, myocardial infarction, or death did not differ significantly between stented patients and those undergoing endarterectomy. Arterial stenosis located more distally and intracranial lesions either are treated with angioplasty alone or are stented following angioplasty. There are no efficacy data available for these more distal lesions, and a recent trial of stenting versus medical therapy for intracranial stenosis found that medical therapy had lower 12-mo rates of stroke and death.

Vasospasm often accompanies subarachnoid hemorrhage and results in ischemic complications, which are a common cause of morbidity and mortality following aneurysmal rupture. The endovascular therapist is often asked to treat this problem with either drugs or balloons. Direct administration of intraarterial vasodilators, such as verapamil, nimodipine, and nicardipine, has been used particularly for treatment of more distal spasm. More proximal spasm involving the arteries of the circle of Willis is often treated using high-compliance angioplasty balloons.

▪ SUMMARY OF PROCEDURES

	Embolization	Aneurysm Therapy	Cerebral Revascularization
Position	Supine	⇚	⇚
Incision	Femoral artery, catheterization (may utilize brachial or radial artery)	⇚	⇚
Unique considerations	BP control; AVM; anticoagulation; EP monitoring	BP control; ± EP monitoring; anticoagulation	⇚
Antibiotics	Usually none; occasionally used with closure device	⇚	⇚
Procedure time	2-5 h	2-4 h	⇚
Closing considerations	Femoral artery compression or closure device	⇚	⇚
EBL	Minimal	⇚	⇚
Postop care	Ward or ICU × 24-48 h	ICU	Ward or ICU
Mortality	1-2% (vascular lesions)	⇚	⇚
Morbidity	Overall: ˜5% Thromboembolic stroke Hemorrhage (AVM, AVF)	⇚ ⇚ SAH	⇚ ⇚ Vessel rupture/dissection
Pain score	1-2	1-2	1-2

ANESTHETIC CONSIDERATIONS

PREOPERATIVE

Patients presenting for diagnostic neuroradiologic procedures frequently may require only local anesthesia and sedation. The newer nontoxic and low osmolality contrast agents have improved patient comfort and tolerance of these
procedures while minimizing adverse reactions. Patients presenting for therapeutic neuroradiological procedures may be restless and are likely to experience some discomfort and, therefore, may require GA to tolerate these often lengthy procedures. The advantages of GA, however, must be balanced against the potential need for intraop neurological monitoring (e.g., speech, vision, and mental status) that requires the patient to be awake and cooperative. In this set of circumstances, close consultation between the neuroradiologist and anesthesiologist is required in formulating the anesthesia plan. In many cases, time is of the essence, and even short delays may reduce favorable outcome.

Respiratory	Access to the airway may be limited; therefore, examination should focus on the need for elective ET intubation. Patients with chronic cough may require GA to ensure immobility. Tests: As indicated from H&P
Cardiovascular	Patients with recent intracranial hemorrhage may demonstrate ECG abnormalities (PVCs in 30-80%; ST-T wave changes in > 50%), which need to be differentiated from new ischemic heart disease (ECHO, cardiac enzymes). Tests: ECG; other tests as indicated from H&P
Neurological	Symptoms vary with the location, size, and type of lesion. Aneurysms seldom produce neurological symptoms unless they leak or rupture, whereas tumors are commonly associated with symptoms of ↑ ICP (HA, N/V, altered mental status, papilledema). Patients with recent cerebral hemorrhages are likely to be medicated with calcium channel blockers (e.g., nimodipine, nicardipine) to ↓ arterial vasospasm. Patients with ↑ ICP or cranial trauma usually will need GA with intubation and mechanical ventilation.
Premedication	Preop sedation may mask the Sx of ↑ ICP or intracranial hemorrhage. Patients at high risk for contrast-media reactions (e.g., patients with previous contrast reaction, allergy to iodine or seafood) should receive prophylactic treatment consisting of prednisone, 50 mg po q 6 h × 3, starting 18 h before the study, and diphenhydramine, 50 mg po/im, 1 h before the procedure.

INTRAOPERATIVE

Anesthetic technique: MAC (see p. B-3) may be adequate for patients undergoing diagnostic procedures and necessary for patients requiring neurological assessment during more invasive procedures; otherwise, use GETA or be prepared to rapidly convert to GETA during the procedure. Although several reports suggest that patients receiving GETA for neurointerventional procedures have worse outcomes compared to those receiving sedation, these observations are not based on randomized controlled studies and are inherently biased because the patients most likely to receive only sedation are also the most likely to be stable and uncomplicated at the time of the procedure.

Induction	Standard induction (see p. B-2). Patients with ↑ ICP should be hyperventilated to an ETCO₂ of ˜30 mm Hg. In patients with vascular lesions that may leak or rupture, BP responses to laryngoscopy and intubation should be blunted (e.g., remifentanil: 3-5 mcg/kg iv 1-2 min in advance).
Maintenance	Standard maintenance (see p. B-3). Muscle relaxation is usually mandatory to control ventilation and minimize the chance of movement. Maintain normocapnia, although hyperventilation may be necessary to ↓ ICP and may also enhance the quality of the angiogram. Heparin (ACT goal: 250-350 sec) may be requested. Protamine should be immediately available.
Emergence	Prompt awakening is important to permit neurologic evaluation. Ondansetron (4 mg iv) is useful to ↓ postop N/V. Extubate when airway reflexes have returned. Continuous control of BP may be necessary during emergence phase. Patients typically are transported to ICU immediately following the procedure.
Blood and fluid requirements	IV: 18 ga × 1-2 NS @ 3-5 mL/kg/h	Avoid glucose-containing solutions unless the patient is hypoglycemic (< 70 mg/dL)
Monitoring	Standard monitors (see p. B-1). Arterial line Urinary catheter ± EPs Glucose	BP can be monitored from femoral line placed by radiologist. However, another arterial line often will be necessary for postop monitoring in the ICU. Place urinary catheter if procedure is lengthy (> 3 h). Keep isoflurane or sevoflurane < 0.5 MAC and N₂O < 50% to minimize interference with EP monitoring. Supplement with remifentanil infusion, if necessary. TIVA may be requested in the erroneous belief that motor or sensory EPs cannot be obtained while using inhalational agents. Keep serum glucose 70-140 mg/dL. Use insulin infusion to control hyperglycemia.
Control of BP	SNP (0.2-2 mcg/kg/min) Maintain normovolemia. Esmolol (50-200 mcg/kg/min)	BP control may be necessary during intracranial catheter manipulation, embolization, and postembolization. Close communication with the radiologist is important. In patient with acute ischemic stroke or intracranial hemorrhage, keep SBP between 140 and 220 mm Hg (140 and 180 mm Hg after iv tPA). SNP/esmolol may be infused through a second peripheral iv.
Positioning	[check mark] and pad pressure points [check mark] eyes	X-ray table may not be well padded → nerve damage.
Complications, contrast related	Common reactions: N/V Itching Urticaria Sensation of warmth Pain Anxiety Rash Neurotoxic Sx: Hemiplegia Blindness Aphasia ↓ consciousness Major allergic reactions: Bronchospasm ↓ BP Cardiac arrest Pulmonary edema Laryngeal edema Dysrhythmias	These reactions occur in > 5% of patients and may require no treatment apart from reassurance or a mild anxiolytic. Mild allergic reactions may be treated with diphenhydramine 25-50 mg iv. Monitor patients for progression of Sx → need for more aggressive therapy. These reactions may be related to the hyperosmolarity of the agent. If persistent, procedure should be terminated. Rx may require steroids and vasopressors to improve perfusion. In the anesthetized patient, these Sx will be masked. Epinephrine (0.25-0.5 mg iv) should be given immediately. Rx of anaphylaxis includes: eliminate antigens (e.g., contrast agent, latex); secure airway; administer 100% O₂, iv fluids, epinephrine, and diphenhydramine + ranitidine. Supplemental Rx may include steroids (e.g., hydrocortisone 5 mg/kg), atropine, NaHCO₃, vasopressin, and epinephrine infusion.
Complications, other	Hemorrhage Vasospasm Occlusion of vessel	Reverse heparin (1 mg protamine/100 mg heparin). Intracranial bleeding may require immediate transport to OR for surgical repair. Rx: vasodilators (e.g., NTG) or papaverine delivered by catheter, or balloon angioplasty. Deliberate hypertension may be beneficial. Rx: angioplasty. (Recanalization and stenting may be used for thrombotic occlusions.)

POSTOPERATIVE

Complications

Neurologic deficits

Vasospasm

CT scan for evaluation, as prompt neurosurgical intervention may be required.

May require Ca⁺⁺ channel blocker (e.g., nimodipine). Consult with neurosurgeon.

Suggested Readings

1. Blackburn SL, Ashley WW Jr, Rich KM, et al: Combined endovascular embolization and stereotactic radiosurgery in the treatment of large arteriovenous malformations. J Neurosurg 2011; 114:1758-67.

2. Brott TG, Hobson RW, Howard G, et al: Stenting versus endarterectomy for treatment of carotid-artery stenosis. NEJM 2010; 363:11-23.

3. Froehler MT, Fifi JT, Majid A, et al: Anesthesia for endovascular treatment of acute ischemic stroke. Neurology 2012; 79: 8167-73.

4. Gahremanpour A, Perin EC, Silva G: Carotid artery stenting versus endarterectomy: a systematic review. Tex Heart Inst J 2012; 39(4):474-87.

5. Gupta R, Vora NA, Horowitz MB, et al: Multimodal reperfusion therapy for acute ischemic stroke: factors predicting vessel recanalization. Stroke 2006; 37:986-90.

6. Hartmann A, Mast H, Mohr JP, et al: Determinants of staged endovascular and surgical treatment outcome of brain arteriovenous malformations. Stroke 2005; 36:2431-5.

7. Jayaraman MV, Marcellus ML, Hamilton S, et al: Neurologic complications of arteriovenous malformation embolization using liquid embolic agents. AJNR Am J Neuroradiol 2008; 29:242-6.

8. Lakhani S, Guha A, Nahser HC: Anaesthesia for endovascular management of cerebral aneurysms. Eur J Anaesthesiol 2006; 23:902-13.

9. Lee CZ, Young WL: Anesthesia for endovascular neurosurgery and interventional neuroradiology. Anesthesiol Clin 2012; 30(2):127-47.

10. Leong S, Fanning NF: Persistent neurological deficit from iodinated contrast encephalopathy following intracranial aneurysm coiling. A case report and review of the literature. Interv Neuroradiol 2012; 18(1):33-41.

11. Marks MP, Wojack JC, Al-Ali F, et al: Angioplasty for symptomatic intracranial stenosis. Stroke 2006; 37:1016-20.

12. Molyneux AJ, Kerr RSC, Ya LM, et al: International subarachnoid aneurysm trial (ISAT) of neurosurgical clipping versus endovascular coiling in 2143 patients with ruptured intracranial aneurysms: a randomised comparison of effects on survival, dependency, seizures, rebleeding, subgroups and aneurysm occlusion. Lancet 2005; 366:809-17.

13. Saatci I, Yanvuz K, Ozer C, et al: Treatment of intracranial aneurysms using the pipeline flow-diverter embolization device: a single-center experience with long-term follow-up results. AJNR 2012; 33:1436-46.

14. Scharf J, Dempfle CE: Anticoagulation in neurointerventions: basic pharmacology and pathophysiology, current status, practical advice. Clin Neuroradiol 2012; 22(1):3-13.

15. Smith WS: Safety of mechanical thrombectomy and intravenous tissue plasminogen activator in acute ischemic stroke: results of the multi Mechanical Embolus Removal in Cerebral Ischemia (MERCI) trial, part 1. AJNR Am J Neuroradiol 2006; 27:1177-82.

16. Smith WS, Sung G, Starkman S, et al: Safety and efficacy of mechanical embolectomy in acute ischemic stroke. Results of the MERCI Trial. Stroke 2005; 36:1432-40.

17. Taqi MA, Vora N, Callison RC, Lin R, Wolfe TJ: Past, present, and future of endovascular stroke therapies. Neurology 2012; 79(13 Suppl 1):S213-20.

DIRECT CURRENT (DC) CARDIOVERSION

PROCEDURAL CONSIDERATIONS

Description: Direct current (DC) cardioversion is a treatment for cardiac arrhythmias that uses a brief, dosed discharge of electricity across the heart. This biphasic waveform energy is more efficient, requiring 20-170 J, than monophasic waveform, which requires 50-360 J. Effective depolarization of a critical mass of the heart terminates the arrhythmia, allowing NSR to resume. The electrical shock is delivered across the chest wall, using two external paddles placed in one of the standard positions (i.e., the anterior-posterior [A-P], basilar-apical, or apical-posterior). The pulse is delivered synchronous to the QRS, thus avoiding the vulnerable period for inducing malignant tachyarrhythmias. Shock to treat ventricular fibrillation is applied emergently and asynchronously (thus, the term “defibrillation”). To avoid discomfort, cardioversion should always be performed with the patient under deep sedation or brief GA. It is unacceptable to deliver this therapy to an awake patient.

Usual preop diagnosis: Atrial fibrillation (AF); atrial flutter; other supraventricular tachyarrhythmias; ventricular tachyarrhythmias

▪ SUMMARY OF PROCEDURE

Position	Supine with defibrillator pads positioned A-P, basilar-apical, or apical-posterior
Unique considerations	Adequate anticoagulation (INR = 2-3) in patients with AF
Antibiotics	None
Procedure time	≤ 30 min
Postop care	Monitoring of cardiac rhythm in treatment room
Mortality	0.1%
Morbidity	Skin burns: < 15% (1st degree); 2% (2nd degree); lesser incidence with biphasic waveform Embolic event: 2% (↑ risk with mitral valve disease) Acute pulmonary edema: 1% More serious arrhythmia: 1% Myocardial damage: Incidence unknown, but estimated to be very low—proportional to delivered energy.
Pain score	2-3

ANESTHETIC CONSIDERATIONS

PREOPERATIVE

In general, patients presenting for cardioversion fall into one of two categories: elective or emergent. The presence or absence of hemodynamic instability will define the category. In the emergency patient, full-stomach precautions may be necessary (see p. B-5). Elective cardioversions usually are carried out on patients who have failed drug therapy.

Respiratory	Preop evaluation of the airway should focus on the need for elective ET intubation (patients with GERD, difficult mask fit, or airway compromise).
Cardiovascular	Relative contraindications to elective cardioversion include digitalis toxicity (toxic = > 3 ng/mL), ↓ K⁺, inadequate anticoagulation, presence of β-blockade, AV block. The presence of significant CHF, CAD, or valvular disease may predispose this patient population to ↓↓ BP in response to anesthetic agents. Consider use of etomidate (0.1-0.2 mg/kg). Patients at ↑ risk for embolization include those with Hx of embolization within 2 yr, mitral stenosis, intraarterial thrombus, CHF, or hyperthyroidism. In these patients, ensure adequate anticoagulation (PT 1.5-2 × baseline, INR 2.0-3.0). It has been suggested that NTG patches near the electrodes be removed prior to cardioversion to avoid risk of explosion. Tests: ECG; TEE ([check mark] for thrombus and size of atrium); digitalis level (toxic = > 3 ng/mL → refractory VF following cardioversion); electrolytes; INR.
Endocrine	Hyperthyroidism → AF
Gastrointestinal	Full-stomach precautions (see p. B-5) may be necessary in the emergency patient.
Neurological	[check mark] Hx for TIAs or CVAs →↑ risk of embolic event. Pre- and postprocedure neurologic exams should be done.
Hematologic	[check mark] need for anticoagulation (see above).
Laboratory	Other tests as indicated from H&P
Premedication	Usually not needed. For the emergency patient, take full-stomach precautions (see p. B-5).

INTRAOPERATIVE

Anesthetic technique: Brief GA with mask oxygenation and ventilation

Induction	Preoxygenate patient. For hemodynamically fragile patients, etomidate (0.1-0.2 mg/kg iv) is the agent of choice (NB: etomidate-induced clonus → ECG artifact). For the hemodynamically stable patient, use propofol (1.0-1.5 mg/kg iv slowly) until loss of lid reflex. Additional analgesia may be provided by remifentanil (1-2 mcg/kg iv), thereby reducing anesthetic requirements.
Maintenance	Occasionally necessary to repeat cardioversion. Additional small doses of propofol, etomidate, or remifentanil may be required.
Emergence	Patients should awaken rapidly with full recovery of airway reflexes. Outpatients are usually discharged to home within 1-2 h.
Blood and fluid requirements	No blood loss IV: 20 ga × 1 NS/LR @ TKO
Monitoring	Standard monitors (see p. B-1).	Avoid placement of ECG electrodes in precordial area.
Positioning	Hospital bed, supine	Procedure takes place at patient’s bedside.
Complications	Loss of airway VF ↑↑ BP/myocardial ischemia Severe bradycardia Thermal injury ↓ CO	Use airway manipulation ± artificial airways; be prepared to intubate. Use ACLS protocols. Cardioversion → catecholamine surge → acute MI in susceptible patient population. Rx: Atropine (e.g., 0.4 mg iv) Ensure good electrode/skin contact. 2° anesthetic drugs or myocardial stunning from cardioversion. Rx: inotropic support (e.g., ephedrine)

POSTOPERATIVE

Complications

Recall

Systemic embolization

↓ BP/↓ CO/CHF

New dysrhythmia

Renal dysfunction

Especially in hemodynamically fragile patients. Discuss possibility with patient in advance.

Neurological exam should be repeated postcardioversion. Atrial contraction may not be effective following cardioversion →↓ CO/↓ BP.

Incidence: 17%. ↓ renal function labs.

Pain management

Minimal

Myalgias not uncommon; consider ketorolac.

Tests

ECG

Verify NSR.

Suggested Readings

1. Dell’Orfano JT, Naccarelli GV: Update on external cardioversion and defibrillation. Curr Opin Cardiol 2001; 16(1):54-7.

2. Hellman Y, Cohen MJ, Leibowitz D, et al: The incidence and prognosis of renal dysfunction following cardioversion of atrial fibrillation. Cardiology 2013; 124(3):184-9.

3. Hullander RM, Leivers D, Wingler K: A comparison of propofol and etomidate for cardioversion. Anesth Analg 1993; 77(4): 690-4.

4. Santini L, Forleo GB, Topa A, et al: Electrical cardioversion of atrial fibrillation: different methods for a safe and effective technique. Expert Rev Cardiovasc Ther 2005; 3(4):601-10.

IMPLANTATION OF CARDIOVERTER-DEFIBRILLATOR (ICD) OR CARDIAC RESYNCHRONIZATION THERAPY DEFIBRILLATOR (CRT-D)

PROCEDURAL CONSIDERATIONS

Description: The implantable cardioverter-defibrillator (ICD) is an effective device for the prevention of premature death from ventricular tachycardia (VT) or ventricular fibrillation (VF). The results of randomized trials involving survivors of cardiac arrest and those considered at risk for sudden death showed the superiority of ICD therapy over conventional medical therapy in lowering the incidence of sudden death and overall mortality. The MADIT II trial showed the device therapy to be advantageous over standard medical therapy in patients with low LVEF (< 30%). Over the past decade, significant advances have occurred in ICD technology. The devices have decreased dramatically in size (now < 30 cc) along with substantial increases in functionality. Newer devices can incorporate the full capabilities of a permanent pacemaker for bradycardia support and resynchronization therapy, as well as hemodynamic monitoring. Therapies for atrial tachyarrhythmias (atrial tachycardia and fibrillation) are also available in select devices. The more efficient biphasic waveform, which results in a much lower defibrillation threshold (DFT) and, hence, lowers required energy delivery and storage, is now standard for all ICDs. Implantation of these small ICDs results in mortality and morbidity rates very similar to those associated with standard pacemaker implantation.

The device system consists of a small pulse generator and transvenous leads that are designed to record ventricular depolarizations and deliver a shock via coils or patches. ICD terminates VT/VF by sensing these rhythms and responding with an appropriate countershock. The most common ICD implantation uses endocardial leads inserted percutaneously (transvenous approach) via pectoral (or, rarely, abdominal) subcutaneous/submuscular pulse generator placement. In the unusual circumstances of difficult endocardial access or high DFT (> 25 J), additional leads can be placed either in the coronary sinus or subcutaneously. Very rarely would the leads (in the form of patches) be applied epicardially via a thoracotomy approach.

In the transvenous approach, the insertion of leads and pulse generator requires minimal anesthesia; however, during testing of defibrillation efficacy, VF is induced once or twice and sometimes more frequently. Thus, in addition to continuous monitoring of VS and cardiac rhythm, the anesthesiologist should pay special attention to the patient’s hemodynamic stability prior to VF induction and after the defibrillation. In the event of failed defibrillation by the programmed first shock, a somewhat prolonged VF may occur. In the case of repeated DFT testing, it is customary to give at least 5-min intervals between VF inductions to allow for sufficient hemodynamic recovery. In patients with significant LV dysfunction, ↓ BP is not uncommon, but caution should be taken with fluid administration. If recovery from ↓ BP is slow, complications such as pneumo/hemothorax or pericardial effusion/tamponade should be considered. In the absence of a PA catheter (which would interfere with ICD lead positioning), accurate assessment of hemodynamic status is limited. Thus, meticulous attention should be directed at arterial pressure, HR, and oxygenation status. Finally, it is not uncommon to encounter acute atrial fibrillation (AF) from induction and conversion of VF. Fortunately, a cardioversion can be applied easily, using the ICD itself or relying on the external rescue system (external cardioversion).

The cardiac resynchronization therapy defibrillator (CRT-D) was developed for heart failure (HF) patients with electrical and/or mechanical dyssynchrony, typically those with intraventricular conduction delay of LBBB type where the delay causes a mechanical dyssynchrony that increases systolic inefficiency. This form of therapy, in addition to preventing premature sudden death from VT or VF, has been shown to reverse ventricular remodeling and improve objective and subjective measure of HF. This form of therapy requires implantation of a left-ventricular lead into one of the tributaries of the coronary sinus system.

Figure 13.1-2. Induced VF (with underlying AF) is shown on top panel, whereby the first (24-J) shock failed to terminate VF but terminated AF (as indicated by the ICD annotation). The second shock (34-J) terminated VF, resulting in V-paced rhythm with underlying sinus and AV block. Total down-time during VF was 16 sec. Downtime is dependent on the detection time and charge time, which, in turn, depend on the energy programmed.

There are significant differences between ICD/CRT-D implantation and pacemaker implantation. Patients undergoing ICD/CRT-D implantation typically have moderate or severe HF, and their tolerance to sedation may be limited. ICD/CRT-D implantation usually requires induction of VT/VF to assess defibrillation threshold (DFT), which requires a transiently deeper level of sedation. An alternative to VT/VF induction is now available using the Upper Limit of Vulnerability (ULV) method, whereby estimated defibrillation energy is delivered on the vulnerable T-wave period and a failure to induce VF is accepted as the equivalent to the DFT. Nonetheless, VF induction should be anticipated and prepared for. Finally, in CRT-D implantation, the placement of left ventricular lead within a coronary vein tributary may require a significantly longer time than a simple pacemaker implantation.

Usual preop diagnosis: Documented, induced, or high-risk ventricular fibrillation; moderate-severe heart failure

▪ SUMMARY OF PROCEDURE

Position	Supine with defibrillator pads positioned A-P or basilar-apical
Incision	Left pectoral or abdominal
Special instrumentation	ICD pulse generator, lead(s), and testing system (manufacturer-specific)
Unique considerations	Multiple inductions of VT/VF with associated ↓ CO, ↓ BP
Antibiotics	Standard iv antimicrobial for staphylococcus/streptococcus organism
Surgical time	1-2 h (more for ICD with cardiac resynchronization [CRT])
Closing considerations	Routine subcutaneous/submuscular pocket closure
EBL	5-20 mL
Postop care	Monitoring of arrhythmia, pocket bleeding/hematoma, pneumothorax
Mortality	0.1% (transvenous); ≤ 5% (thoracotomy)
Morbidity	New-onset arrhythmias: ≤ 5% Pneumothorax: ≤ 5% (transvenous) Pericardial effusion/tamponade: ≤ 1% (transvenous)
Pain score	3 (6-9, thoracotomy)