<<

Arrhythmias in the intensive care patient Hans-Joachim Trappe, Bodo Brandts and Peter Weismueller

Purpose of review ventricular fibrillation. The use of automatic external , , AV–nodal reentry tachycardia defibrillators by basic life support ambulance providers or first with rapid ventricular response, atrial ectopic tachycardia, and responder in early defibrillation programs has been associated preexcitation syndromes combined with atrial fibrillation or with a significant increase in survival rates. Drugs such as ventricular tachyarrhythmias are typical in intensive , , , , or care patients. Most frequently, the diagnosis of the underlying were recommended for treatment of ventricular is possible from the physical examination, the tachyarrhythmias in intensive care patients. Amiodarone is a response to maneuvers or drugs, and the 12-lead surface highly efficacious for many cardiac electrocardiogram. In all patients with unstable hemodynamics, arrhythmias, ranging from atrial fibrillation to malignant immediate DC- is indicated. Conversion of atrial ventricular tachyarrhythmias, and seems to be superior to other fibrillation to sinus rhythm is possible using antiarrhythmic antiarrhythmic agents. drugs. Amiodarone has a conversion rate in atrial fibrillation of up to 80%. However, caution in the use of short-term Keywords administration of intravenous amiodarone in critically ill patients atrial fibrillation, arrhythmias, amiodarone, ibutilide, automatic with recent-onset atrial fibrillation is absolutely necessary, and external defibrillators the duration of therapy should not exceed 24 to 48 hours. Ibutilide represents a relatively new class III antiarrhythmic Curr Opin Crit Care 9:345–355. © 2003 Lippincott Williams & Wilkins. agent that has been reported to have conversion rates of 50% to 70%; it seems that ibutilide is even successful when Department of Cardiology and Angiology, Ruhr-University Bochum, Germany intravenous amiodarone failed to convert atrial fibrillation. Recent findings Correspondence to Hans-Joachim Trappe, MD, Department of Cardiology and Angiology, Ruhr-University Bochum Hoelkeskampring 40, 44625 Herne, Germany Newer studies compared the outcome of patients with atrial E-mail: [email protected] fibrillation and rhythm- or rate-control. Data from these studies Current Opinion in Critical Care 2003, 9:345–355 (AFFIRM, RACE) clearly showed that rhythm control is not superior to rate control for the prevention of death and © 2003 Lippincott Williams & Wilkins 1070-5295 morbidity from cardiovascular causes. Therefore, rate-control may be an appropriate therapy in patients with recurrent atrial fibrillation after DC-cardioversion. Acute therapy of atrial flutter in intensive care patients depends on the clinical presentation. Introduction Atrial flutter can most often be successfully cardioverted to Emergency medicine and critical care are fields that sinus rhythm with energies less than 50 joules. Ibutilide trials often require rapid diagnosis and intervention for spe- showed efficacy rates of 38–76% for conversion of atrial cific situations [1]. These critical interventions can be flutter to sinus rhythm compared with conversion rates of life-saving or severely debilitating, depending on their 5–13% when intravenous , , or appropriateness and timeliness. In cardiac emergencies, was administered. In addition, a high dose (2 mg) of accurate differentiation of ventricular and supraventricu- ibutilide was more effective than sotalol (1.5 mg/kg) in lar tachyarrhythmias is essential for appropriate manage- conversion of atrial flutter to sinus rhythm (70% versus 19%). ment [2]. Most frequently, the diagnosis of the underly- Summary ing arrhythmia is readily apparent, but occasionally it is There is general agreement that bystander first aid, necessary to use clues from the physical examination, defibrillation, and advanced life support is essential for the response to maneuvers or drugs, in addition to the neurologic outcome in patients after cardiac arrest due to 12-lead surface electrocardiogram [3,4]. Treatment of ventricular tachyarrhythmias. The best survival rate from cardiac arrhythmias in intensive care and emergency cardiac arrest can be achieved only when (1) recognition of medicine is sometimes difficult. Correct therapy based early warning signs, (2) activation of the emergency medical on an understanding of the mechanism that caused the services system, (3) basic cardiopulmonary resuscitation, arrhythmia may not only be lifesaving in the immediate (4) defibrillation, (5) management of the airway and ventilation, situation, but may also improve the quality of life. The and (6) intravenous administration of medications occurs as purpose of the present chapter is to summarize new rapidly as possible. Public access defibrillation, which places strategies for patients with supraventricular or ventricu- automatic external defibrillators in the hands of trained lar tachyarrhythmias in intensive care or cardiac emer- laypersons, seems to be an ideal approach in the treatment of gencies. 345 346 Cardiovascular system

Types of tachyarrhythmias rhythmia episodes were assessed during the study period Supraventricular tachyarrhythmias include atrial fibrilla- in 133 patients, with a mean of 2.91 episodes per patient tion, atrial flutter, AV-nodal reentrant tachycardia with (range 1–14). Admission diagnoses were cardiac (n = 48), rapid ventricular response, atrial ectopic tachycardia, and cardiac surgery (n = 45), resuscitation (n = 12), pulmonary preexcitation syndromes combined with atrial fibrilla- (n = 15), sepsis (n = 5), neurologic (n = 2), and others tion. Ventricular tachyarrhythmias still remain the main (n = 6). Among the 310 arrhythmia episodes, there were cause of death; these arrhythmias include monomorphic 278 tachycardia (179 episodes regular, 97 episodes irreg- and polymorphic , torsade de pointes ular) and 32 bradycardia events (heart rate <40 beats/min). tachycardia, ventricular flutter, and ventricular fibrilla- There were 108 narrow-QRS complex tachycardia and tion. In the assessment of patients with life-threatening 168 wide-QRS complex tachycardia with two episodes of supraventricular or ventricular arrhythmias, attention primary ventricular fibrillation. Among the 278 tachycar- should be given to identify whether the tachycardia is dias, 135 episodes (48.6%) were ventricular, 13 episodes associated with worsening angina or low cardiac output. (4.7%) were torsade de pointes tachycardia, and 83 epi- There is general agreement that many cardiac or extra- sodes (29.8%) were atrial fibrillation, 10 episodes were cardiac causes can lead to supraventricular or ventricular atrial flutter (3.6%), 21 were supraventricular tachycardia tachyarrhythmias and to cardiac arrest; left ventricular (7.6%), and 2 were ectopic atrial tachycardia (0.7%). It function (or dysfunction) plays an important role in prog- seems that in critically ill patients, two types of arrhyth- nosis and outcome (Fig. 1). mias are dominantly visible: sustained ventricular tachy- cardia and atrial fibrillation. Lampert and Ezekowitz re- Incidence and type of cardiac arrhythmias ported recently that the aging heart is susceptible to in critically ill or elderly patients diverse cardiac arrhythmias, and in many of these ar- It has been well known for many years that cardiac ar- rhythmias intensive care medicine is mandatory [6]. rhythmias can occur in healthy people or in patients with Baine et al. studied the incidence of arrhythmia types, cardiac or extracardiac diseases. Arrhythmias are well de- hospital and intensive care stay in 144,512 elderly pa- fined in patients after , in patients tients (age 65 years or older) with cardiac arrhythmias with underlying cardiac or pulmonary disease, and in (time interval 1991–1998) [7]. In 1998, atrial fibrillation patients after cardiac surgery or heart transplantation [5]. was the most frequent arrhythmia and accounted for However, only few data are available regarding incidence 44.8% of the relevant discharges. Atrial flutter was ob- and type of arrhythmias in critically ill patients. Reinel et served in 5.2%, sinoatrial node dysfunction in 13.2%, and al. studied all consecutive arrhythmia episodes in criti- complete AV block in 5.8%. Supraventricular tachycardia cally ill patients in a medical–cardiologic intensive care was observed in only 3.8%. Cardiac arrest was present in unit between 1996 and 1999 [5]. All episodes of patients 1.3%, ventricular tachycardia in 6.9%, and ventricular fi- with new-onset, sustained arrhythmias (duration Ն30 brillation in 1.3%. It is interesting to note that lengths of seconds) were included that were either self-term- stay in hospital and intensive care are determined by the inated or that required intervention. A total of 310 ar- underlying arrhythmia: mean hospital stay was 7.8 days

Figure 1. Diagnostic methods in intensive care patients after cardiac arrest caused by ventricular fibrillation Mechanisms and diagnostic methods in intensive care patients after cardiac arrest caused by ventricular fibrillation. Angio, angiography; BRS, baroreflex sensitivity; ECG, electrocardiogram; EPS, programed electrical stimulation; HRV, heart rate variability; LVEF, left ventricular ejection fraction. Arrhythmias in intensive care patient Trappe et al. 347 in ventricular fibrillation, 7.0 days in ventricular tachy- Acute management cardia in contrast to 4.7 days in atrial fibrillation, 4.5 days Atrial fibrillation or flutter is the most frequent arrhyth- in atrial flutter, or 5.6 days in complete AV block. Mean mia in emergency rooms and intensive care units, both in intensive care stay was 2.7 days in ventricular fibrillation, surgical and cardiologic intensive care units [8]. Knotzer 1.7 days in ventricular tachycardia, 0.9 days in atrial fi- et al. found that 14.8% of surgically ill patients developed brillation, 1.0 days in atrial flutter, or 1.5 days in com- atrial tachyarrhythmias compared with 47.4% of patients plete AV block. In addition to the study by Reinelt et al., treated in a cardiologic intensive care unit [5,9]. The goal management of atrial fibrillation is also a major problem of acute treatment of atrial fibrillation with rapid ven- in elderly patients. tricular response is to restore sinus rhythm or to control the ventricular rate (Fig. 2). If cardioversion to sinus rhythm is not possible, the secondary goal is to slow the Atrial fibrillation ventricular response, usually to a rate of less than 100 beats Since the time of Hippocrates, there has been interest per minute. Patients who are hemodynamically unstable in how the heartbeat is initiated. It was concluded that (significant hypotension, severe angina, pulmonary the nervous system initiates the heartbeat. In 1907, edema) should be promptly cardioverted after adminis- Keith and Flack described the sinus node and suggested tration of an anesthetic agent. Cardioversion should al- it as the site of initiation within the atrium. It became ways be performed in a synchronized mode. clear that electrical disturbances in the atrium (disrup- tions in the normal spread of activation) will lead to atrial Hemodynamically stable situation: restoration of arrhythmias. Clinical, there is an increased interest in sinus rhythm atrial arrhythmias, particularly atrial fibrillation, because In patients in whom atrial fibrillation is of known acute the incidence of this arrhythmia is high and the associ- onset (present for less than 48 hours) DC-cardioversion ated morbidity and mortality higher than previously should be considered early. Pharmacologic conversion to recognized. sinus rhythm with antiarrhythmic drugs is a widely used

Figure 2. Stored electrocardiogram in a patient with an implanted automatic cardioverter defibrillator

Patient was admitted to an intensive care unit because of frequent episodes of implanted automatic cardioverter defibrillator (ICD) discharges. The electrocardiogram clearly shows atrial fibrillation with rapid ventricular response (heart rate 175 beats per minute) without successful ICD therapy. Postshock persistence of atrial fibrillation with a heart rate of 187 beats per minute. 348 Cardiovascular system therapeutic alternative with different efficacy rates [10]. these studies are not performed in critically ill patients, Amiodarone has a conversion rate in atrial fibrillation of they have many implications for the management of pa- up to 80% [11]. However, only a single retrospective tients with atrial fibrillation, arriving in an intensive care study has been published that includes intensive care unit. A total of 4060 patients (mean age 69.7 ± 9.0 years) unit patients with left ventricular dysfunction, although with atrial fibrillation and a higher risk of stroke or death this is frequent in critically ill or even in elderly patients were enrolled in the AFFIRM study [16•]. Patients were with recent onset of atrial fibrillation [12]. In critically ill assigned to rhythm-control (2033 patients) or to rate- patients, amiodarone is indicated for a wide range of control therapy (2027 patients). The primary endpoint of arrhythmias including recent-onset atrial fibrillation. De- this study was overall mortality. In the rhythm-control spite many published reports on safety and efficacy of group, more than two thirds of patients started therapy intravenous amiodarone in the treatment of patients with with amiodarone or sotalol. By the end of the study al- recent-onset atrial fibrillation, there are an increasing most two thirds of the patients in this group had under- number of reports in critically ill patients highlighting gone at least one trial of amiodarone. In the rate-control occasional serious acute pulmonary toxicity [13]. There- group, beta-blocking agents were used initially in nearly fore, caution in the use of short-term administration of one half of the patients, and of the calcium-channel intravenous amiodarone in the critically ill patient with blockers, was used more frequently than vera- recent-onset atrial fibrillation is absolutely necessary, pamil. In this study, there were 356 deaths among and the duration of therapy should not exceed 24 to the patients assigned to rhythm-control therapy and 48 hours, except when absolutely necessary. In contrast 310 deaths among patients assigned to rate-control to amiodarone, ibutilide represents a relatively new class therapy (P = 0.08). The prevalence of sinus rhythm in III antiarrhythmic agent that has been reported to have the rhythm-control group at follow-up was 82.4%, 73.3%, high conversion rates [14]. Proarrhythmic effects occur in and 62.6% at 1, 3, and 5 years, respectively. In the rate- 5 to 8% of patients, and careful monitoring is required. control group, at 5 years, 34.6% of the patients were in The conversion rates of recent-onset atrial fibrillation to sinus rhythm, and over 80% of those in the atrial fibril- sinus rhythm with ibutilide range from 50 to 70%, and it lation group had adequate heart rate control. More pa- seems that ibutilide is even successful when intravenous tients in the rhythm-control group than in the rate-control amiodarone failed to convert atrial fibrillation [15]. Hen- group were hospitalized, and there were more adverse nersdorf et al. studied 26 patients in whom atrial fibrilla- drug effects in the rhythm-control group as well. In both tion or flutter persisted for a maximum of 6 hours. All groups, most strokes occurred after warfarin had been patients initially received amiodarone (150 mg IV) and stopped or when the international normalized ratio was after 2 hours of persistent arrhythmia ibutilide (1 mg IV; subtherapeutic. From this study it seems clear that man- in the case of persisting arrhythmia and body weight agement of atrial fibrillation with the rhythm-control > 70 kg, a second infusion of 1 mg ibutilide was admin- strategy offers no survival advantage over the rate-control istered after 30 minutes). Before the administration of regimen. In the RACE study, 522 patients with persistent ibutilide, magnesium (1 g) was administered, and high atrial fibrillation after a previous electrical cardioversion normal levels of potassium serum levels were achieved were randomized to a rhythm-control (266 patients) or a (4.5 to 5.0 mmol/L). After amiodarone administration, rate-control group (256 patients) [17••]. The endpoint atrial flutter persisted in 73% and atrial fibrillation in was a composite of death from cardiovascular causes, 27% of patients. After administration of ibutilide, con- heart failure, thromboembolic complications, bleeding, version to sinus rhythm was achieved in 82% patients implantation of a pacemaker, and severe adverse effects after a median time of 7 minutes (range 3 to 12 minutes). of drugs. Patients in the rhythm-control group were The rate of cardioversion with ibutilide was higher treated with sotalol (160 to 320 mg daily), flecainide (200 in atrial flutter (84% patients) than in atrial fibrillation to 300 mg daily), or propafenone (450 to 900 mg daily). If (71% patients). Therefore, in implanted automatic car- there was a recurrence within 6 months after start of the dioverter defibrillator patients with atrial fibrillation or drug treatment, a loading dose of amiodarone was given flutter, ibutilide is an effective drug even when amioda- (600 mg daily for 4 weeks) and thereafter continued with rone failed. Ibutilide seems to be well suited for cardio- 200 mg daily. Rate control was achieved with the admin- version of recent-onset atrial fibrillation or flutter [15]. istration of digitalis, blockers, and beta- blocking agents, alone or in combination. After a mean of Hemodynamically stable situation: rate control or 2.3 ± 0.6 years, 39% of patients in the rhythm-control rhythm control? group had sinus rhythm, as compared with 10% of pa- In every intensive care unit, there are many patients with tients in the rate-control group. The primary endpoint recent-onset atrial fibrillation. Within the last few years, occurred in 22.6% of patients in the rhythm-control cardioversion to sinus rhythm was the goal to treat these group and in 17.2% of patients in the rate-control group. patients. However, there are new important studies re- The distribution of the various components of the pri- porting the role of rate control in these patients: the mary endpoint was similar between both groups. Data AFFIRMand the RACE studies [16•,17•]. Although from this study clearly showed that rhythm control is not Arrhythmias in intensive care patient Trappe et al. 349 superior to rate control for the prevention of death and zem or amiodarone. Although diltiazem allowed signifi- morbidity from cardiovascular causes. Therefore, rate cantly better 24-hour heart rate control, this effect was control may be an appropriate therapy in patients with a offset by a significantly higherincidence of hypotension recurrence of atrial fibrillation after electrical cardioversion. requiring discontinuation of the drug. It seems clear that amiodarone may be an alternative in patients with severe Alternatives for rate control in atrial fibrillation with hemodynamic compromise. rapid ventricular response Both a loss of atrial synchrony and the rapid ventricular Atrial flutter response may be poorly tolerated in hemodynamically Acute therapy for patients with atrial flutter in intensive compromised patients [3]. Attempts to restore sinus care depends on the clinical presentation. If the patient rhythm are frequently unsuccessful or (after AFFIRM presents with acute hemodynamic collapse or congestive and RACE) even debatable [16•,17••]. Heart rate con- heart failure, emergent direct-current synchronized trol becomes the main therapeutic goal in this situation. shock is indicated. Atrial flutter can most often be suc- The optimal regimen for pharmacologic rate control dur- cessfully cardioverted to sinus rhythm with energies less ing atrial fibrillation in critically ill patients is unclear. It than 50 joules. A number of drugs have been shown to be has been well known for many years that treatment with effective in conversion of atrial flutter to sinus rhythm. intravenous , verapamil, beta-blocking agents, or Placebo-controlled intravenous ibutilide trials showed diltiazem is effective in patients with atrial fibrillation efficacy rates of 38 to 76% for conversion of atrial flutter and rapid ventricular response [1]. Digoxin may be help- to sinus rhythm [19,20]. For those who responded to ful for rate control, with an initial dose of 0.5 mg. After ibutilide, the mean time interval to conversion was 30 minutes, 0.25 mg digoxin should be administered 30 minutes. In the largest available study, the efficacy of again. In intensive care and emergency medicine, other intravenous ibutilide (76%) was significantly higher than therapeutic strategies are verapamil (5 to 10 mg IV), dil- that of intravenous procainamide (14%) [21]. Several tiazem (20 mg IV), or beta-blocking agents as such as pro- single-blinded, randomized control trials comparing in- pranolol (1 to 5 mg IV, additional infusion of 10 to 120 mg travenous flecainide with either intravenous propafe- per day) and (500 µg/kg over 1 minute, followed none or intravenous verapamil have shown relatively by a 4-minute maintenance infusion of 50 µg/kg/min poor efficacy for acute conversion (5 to 13%); in addition, with further dose adjustment as necessary) [11]. How- the conversion rate of intravenous sotalol varied from 20 ever, beta-blocking agents or calcium channel blockers to 40%, depending on the sotalol dose, but was not dif- may cause additional hypotension. Just recently, Delle ferent from placebo. High dose (2 mg) of ibutilide was Karth et al. compared another pharmacologic approach more effective than sotalol (1.5 mg/kg) in conversion of for rate control in critically ill patients: these authors patients with atrial flutter to sinus rhythm (70% versus studied the role of amiodarone or diltiazem in a prospec- 19%) [22]. tive, randomized trial [18]. Sixty patients with atrial tachy- arrhythmias (atrial fibrillation 57 patients, atrial flutter 2 Narrow-QRS complex tachycardia patients, atrial tachycardia 1 patient) were randomized to Narrow QRS tachycardia is a cardiac rhythm with a rate diltiazem (25 mg bolus followed by a continuous infusion faster than 100 beats per minute and a QRS duration of 20 mg/h for 24 hours) (group I), amiodarone (300 mg of less than 0.12 seconds. The patient with narrow bolus) (group II) or amiodarone (300 mg bolus followed QRS tachycardia usually seeks medical attention be- by 45 mg/h for 24 hours) (group III). The primary end- cause of palpitations, light-headedness, shortness of point was a >30% heart rate reduction within 4 hours. breath, or anxiety. In many patients with narrow-QRS The secondary endpoint was a heart rate <120 beats/min. complex tachycardia, the tachycardia rate is very high Tachyarrhythmias were considered uncontrolled if the (180-240 beats per minute) and therefore, after onset of heart rate was >120 beats/min four hours after study drug the tachycardia the patient will arrive very soon in an administration. The primary endpoint was achieved in intensive care unit for diagnosis and treatment. In inten- 70% of group I patients, 55% of patients in group II, and sive care and emergency medicine, narrow QRS complex in 75% of patients in group III (P = 0.38). In patients tachycardia is a common problem [1]. achieving heart rate control, diltiazem showed a signifi- cantly better rate reduction when compared with group Acute management II and III (P < 0.01). However, premature drug discon- The definitive diagnosis can be made in most of the tinuation due to hypotension was required significantly patients based on 12-lead electrocardiogram and clinical more often in group I (30%) than in group II (0%) or criteria. Acute (and chronic) treatment should be initi- group III (5%) (P < 0.01). Uncontrolled tachyarrhythmias ated based on the underlying mechanism. In regular nar- were observed more frequently in group II (45%) than in row QRS complex tachycardia, vagal maneuvers should group I (0%) or group III (5%). This study shows that be initiated to terminate the arrhythmia or to modify sufficient rate control can be achieved in critically ill AV conduction. If this fails, intravenous antiarrhythmic patients with atrial tachyarrhythmias using either diltia- drugs should be administered for arrhythmia termination 350 Cardiovascular system in hemodynamically stable patients. , calcium ognize high-risk patients with subsequent cardiac arrest. channel blockers, or beta-blocking agents are the drugs Therefore, it is necessary to treat cardiac arrest patients of first choice. The advantage of adenosine relative to in the emergency situation as well as possible and to intravenous calcium antagonists or beta-blockers relates develop algorithms for long-term therapy. to its rapidity of onset and short half-life [3,4]. Longer acting agents (intravenous calcium channel blockers or General considerations beta-blocking agents) are of value, particularly for pa- Approximately 1000 people in the United States experi- tients with recurrences of narrow QRS tachycardia. It is ence cardiac arrest each day, most often as a complication clearly necessary to avoid concomitant use of intravenous of acute myocardial infarction with accompanying ven- calcium channel blockers and beta-blocking agents be- tricular fibrillation or unstable ventricular tachycardia cause of possible increase of hypotensive and/or brady- (Fig. 4). In the year 2000, the American Heart Associa- cardiac effects [23]. tion reported again the chain-of-survival concept, with The “pill-in-the-pocket” concept four links—early access, cardiopulmonary resuscitation, In patients who arrive in an intensive care unit or even in defibrillation, and advanced care—as the way to ap- critically ill patients who develop narrow QRS complex proach cardiac arrest [28,29]. This publication presents tachycardia, the “pill-in-the-pocket” concept may be of the conclusions of the International Guidelines 2000 interest. This concept means single-dose administration Conference on Cardiopulmonary Resuscitation and of the drug only during an episode of tachycardia for the Emergency Cardiovascular Care. It has been pointed out purpose of termination of the arrhythmia when vagal that the highest potential survival rate from cardiac arrest maneuvers alone are not effective. This approach may can be achieved only when the following sequence of be considered for patients with infrequent episodes of events occurs as rapidly as possible: (1) recognition of AV nodal reentrant tachycardia that are prolonged but early warning signs, (2) activation of the emergency yet well tolerated, and obviates exposure of patients to medical services system, (3) basic cardiopulmonary re- chronic and unnecessary therapy between their rare ar- suscitation, (4) defibrillation, (5) management of the air- rhythmic events [24]. However, patients should be free way and ventilation, and (6) intravenous administration of significant left ventricular dysfunction, sinus bradycar- of medications. It is impossible to review all guideline dia, or preexcitation. It has been reported by Musto et al. changes related to basic life support; this has been de- [23] and Alboni et al. [24] that a single dose of flecainide scribed in detail elsewhere [29]. However, it seems im- (3 mg/kg) terminated acute episodes of AV nodal reen- portant to stress some important issues: change ventila- trant tachycardia. Single-dose therapy with diltiazem tion volumes and inspiratory times for mouth-to-mask or (120 mg) combined with (80 mg) was supe- bag mask ventilation without oxygen ventilation should rior to both placebo and flecainide [20]. In addition, long- have a tidal volume of approximately 10 mL/kg (700 to term follow-up of single-dose therapy with diltiazem 1000 mL) over 2 seconds; oxygen supplementation of a plus propranolol was associated with a significant reduc- smaller tidal volume of 6 to 7 mL/kg (approximately 400 tion in emergency room visits. to 600 mL) may be delivered over 1 to 2 seconds. The compression rate for adult cardiopulmonary resuscitation Ventricular tachyarrhythmias should be approximately 100 per minute and the com- One of the most important problems in intensive care, pression–ventilation ratio for one and two rescuers emergency medicine, and cardiac rhythmology is to man- should be 15 compressions to 2 ventilations when the age patients with recurrent ventricular tachycardia, ven- victim’s airway is unprotected (not intubated). tricular flutter, or ventricular fibrillation [25]. Manage- ment of cardiac arrest due to life-threatening ventricular tachyarrhythmias is one of the most important goals in Neurologic outcome these patients to avoid serious problems and to avoid There is general agreement that bystander first aid, de- sudden cardiac death [26]. However, treatment of the fibrillation, and advanced life support are essential for underlying arrhythmia requires correct diagnosis; in most neurologic outcome in patients after cardiac arrest. Bur patients this is possible using the 12-lead surface elec- et al. evaluated the effects of basic life support, time to trocardiogram [27]. Nevertheless, it is necessary to un- first defibrillation, and emergency medical service arrival derstand in every patient why the arrhythmia was initi- on neurologic outcome in 276 patients after cardiac arrest ated and what the trigger of initiation was in any patient [30]. In contrast to intubation (odds ratio 1.08; 95% CI, (Fig. 3). 0.51–2.31; P = 0.84), basic life support (odds ratio 0.44; 95% CI 0.24–0.77; P = 0.004) and time to first defibril- Cardiac arrest lation (odds ratio 1.08; 95% CI 1.03–1.13; P = 0.001) were Patients who are successfully resuscitated from out-of- significantly correlated with good neurologic outcome. In hospital cardiac arrest have a high rate of mortality after addition to the better neurologic outcome, among the hospital discharge. Unfortunately, we are not able to rec- patients who did not receive basic life support, the av- Arrhythmias in intensive care patient Trappe et al. 351

Figure 3. Holter recording in a 64-year-old patient who developed torsade de pointes tachycardia while in intensive care At 11.44 hours, sinus rhythm with deep ST-segment depression is visible combined with some premature ventricular beats. At 11.53 hours, a torsade de pointes tachycardia occurs degenerating into ventricular fibrillation.

erage cost per patient with good neurologic outcome sig- Time to defibrillation is the most important determinant nificantly increased with the delay of the first defibrilla- of survival from cardiac arrest [32]. The earlier the defi- tion (P < 0.001) [30]. The importance of cerebral brillation is performed the better the success rates for perfusion and pressure and cerebral tissue oxygen ten- resuscitation, irrespective of who is doing the first defi- sion during cardiopulmonary resuscitation has been de- brillation [33]. In the last few years, there has been a scribed recently [31]. significant increase in the use of AEDs in early defibril- lation programs in a variety of settings, including hospi- Early defibrillation tals, emergency medical service, police departments, ca- Public access defibrillation, which places automatic sinos, airport terminals, and commercial aircraft, among external defibrillators (AED) in the hands of trained others. In most of these settings, use of AEDs by basic laypersons, has the potential to be the single greatest life support ambulance providers or first responder in advance in the treatment of ventricular fibrillation since early defibrillation programs has been associated with a the development of cardiopulmonary resuscitation. significant increase in survival rates [34–36•]. 352 Cardiovascular system

Figure 4. Holter recording in a patient who had cardiac arrest while in the intensive care unit

Fast monomorphic ventricular tachycardia degenerates into ventricular flutter and ventricular fibrillation. Termination was possible by DC countershock.

World-wide experience 2-year period, 21 persons had nontraumatic cardiac ar- Automatic external defibrillators were used in 105 pa- rest, and 18 of them had ventricular fibrillation. In the tients with ventricular fibrillation occurring in casinos case of four patients with ventricular fibrillation, defibril- [34]. Fifty-six of the patients (53%) survived to discharge lators were neither nearby nor used within 5 minutes, from the hospital. Among the 90 patients whose collapse and none of these patients survived. Three others re- was witnessed (86%), the clinically relevant time inter- mained in ventricular fibrillation and eventually died vals were a mean of 3.5 ± 2.9 minutes from collapse to later, despite the rapid use of a defibrillator within 5 the delivery of the first defibrillation shock, and 9.8 ± 4.3 minutes. Eleven patients with ventricular fibrillation minutes from collapse to the arrival of the paramedics. were successfully resuscitated, including eight who re- The survival rate was 74% for those who received their gained consciousness before hospital admission. No first defibrillation no later than 3 minutes after a wit- shock was delivered in four cases of suspected cardiac nessed collapse and 49% for those who received their arrest, and the device correctly indicated that the prob- first defibrillation after more than 3 minutes. AEDs were lem was not due to ventricular fibrillation. used in a US airline study in 200 patients, including 99 patients with documented loss of consciousness. The ad- Defibrillation in hospitals and intensive care units ministration of shock was advised in all 14 patients with Hospitals need to pay attention to the timeliness of de- documented ventricular fibrillation, and no shock was fibrillation including monitored and unmonitored ward advised in the remaining patients. The first shock suc- settings, intensive care units, and ambulatory care facili- cessfully defibrillated the heart in 13 patients, and defi- ties. There is a prevalent misconception that hospitals brillation was withheld in one patient at the family’s inherently provide rapid defibrillation followed by request [35]. Recently, Caffrey et al. reported the public prompt advanced life support. In addition, many hospi- use of AEDs in three Chicago airports [36•]. During a tals both in the United States and in Europe have been Arrhythmias in intensive care patient Trappe et al. 353 slow to accept and implement the readily available tech- the same indication as flecainide and is acceptable for nology that allows defibrillation to be performed before treatment of both supraventricular and ventricular tachy- arrival of a physician. Until recently, hospitals and inten- cardia. Because of significant negative inotropic effects, sive care units have been staunchly reluctant to evaluate propafenone and flecainide should be not given to pa- critically their process for providing early defibrillation tients with impaired left ventricular function. In addi- [37]. It is well known from previous studies that delays of tion, both propafenone and flecainide should be avoided 5 to 10 minutes can be expected before the conventional when coronary artery disease is suspected. in-hospital code teams deliver the first shock to patients with ventricular fibrillation. It has been shown that Class III drugs nurses in the hospital setting can be easily trained to use Sotalol prolongs duration and increases an AED and to safely and effectively operate the device. cardiac tissue refractoriness. In addition, it has nonselec- tive beta-blocking properties. Sotalol is effective in both Role of antiarrhythmic drugs in intensive supraventricular and ventricular tachycardia. Side effects care and emergencies include bradycardia, hypotension, and torsade de pointes Prompt cardiopulmonary resuscitation and early defibril- tachycardia. Intravenous sotalol in intensive care medi- lation either by DC-countershock or an AED signifi- cine is limited by its need to be infused relatively slowly. cantly improve the likelihood of successful resuscitation This may be impractical and has uncertain efficacy in from ventricular fibrillation [38]. Despite these circum- emergent circumstances, particularly under compro- stances, there is still a place for antiarrhythmic drugs to mised circulatory conditions [29]. Amiodarone is a complex treat patients with life-threatening ventricular tachyar- drug with effects on sodium, potassium, and calcium rhythmias such as monomorphic or polymorphic ven- channels as well as alpha- and beta-adrenergic-blocking tricular tachycardia in intensive care or emergencies [4•]. properties. Amiodarone is a highly efficacious antiar- The American Heart Association has clearly defined rhythmic agent for many cardiac arrhythmias, ranging when and how to use these agents [29]. Drugs such as from atrial fibrillation to malignant ventricular tachyar- lidocaine, procainamide, sotalol, amiodarone, or magne- rhythmias [39]. In most published studies, intravenous sium were recommended for treatment of ventricular amiodarone has been administered in patients with ven- tachyarrhythmias in intensive care or emergencies. tricular tachyarrhythmias only after failure of other anti- arrhythmic drugs. In 1999, Kudenchuk described in 504 Class I drugs randomized patients with out-of-hospital cardiac arrest In summary, there is still a place for lidocaine in the due to refractory ventricular arrhythmias (ARREST treatment algorithm for stable, monomorphic, or poly- study) that treatment with amiodarone (single 300-mg morphic ventricular tachycardia, and lidocaine is accept- dose of intravenous amiodarone) resulted in a higher rate able for these arrhythmias with normal or impaired cardiac of survival to hospital admission (44%) compared with function. In contrast, there is little evidence supporting a placebo (34%) (P = 0.03) [40]. The role of amiodarone benefit from treatment with lidocaine for cardiac arrest. as an emergency drug has been reported recently by Lidocaine seems to be more effective during acute myo- Taylor [39]. cardial infarction. However, the US guidelines postu- lated that lidocaine is a second-tier choice and other drugs are preferred over lidocaine in each ventricular Magnesium tachycardia scenario. In addition, the prophylactic use of Severe magnesium deficiency is associated with cardiac lidocaine is not recommended. Use of procainamide is arrhythmias, symptoms of heart failure, and sudden car- indicated in patients with ventricular tachycardia and is diac death. Hypomagnesemia can precipitate refractory an alternative in pulseless ventricular tachycardia/ven- ventricular fibrillation and can hinder the replenishment tricular fibrillation. Its utility in pulseless cardiac arrest is of intracellular potassium. Magnesium deficiency should less well studied and limited by the need for a relatively be corrected in intensive care and emergencies if pres- slow infusion (maximum rate 50 mg/min) and the achieve- ent. Magnesium is not usually categorized as an antiar- ment of potentially toxic concentrations if administered rhythmic agent. However, it has been known for a long more rapidly. Procainamide should be avoided in pa- time that in emergent circumstances, magnesium sulfate tients with preexisting QT prolongation and torsade de 1to2gishelpful to suppress life-threatening ventricular pointes tachycardia. The electrocardiogram and blood tachyarrhythmias and should be administered over 1 to pressure must be monitored continuously during pro- 2 minutes [4•]. The role of magnesium in intensive care cainamide administration. Precipitous hypotension may and emergency medicine was described by Kaye and occur if the drug is injected too rapidly [29]. Propafenone O’Sullivan in 2002 [41]. These authors concluded that and flecainide are class I antiarrhythmic drugs with sig- magnesium should be the first-line therapy in eclampsia nificant conduction-slowing and negative inotropic ef- and torsade de pointes tachycardia. Data from other stud- fects. In addition, propafenone has nonselective beta- ies show that magnesium has a clearly defined role as a blocking properties. Intravenous propafenone is used for second-line therapy in acute severe bronchial asthma 354 Cardiovascular system

[42]. Hypomagnesemia should be considered in patients References and recommended reading with biventricular failure presenting with malignant ven- Papers of particular interest, published within the period of review, have tricular tachyarrhythmias. Magnesium should be consid- been highlighted as: ered as a temporizing measure in cases of severe digoxin • Of special interest •• Of outstanding interest toxicity while using antibodies as the specific antidote. 1 Trappe HJ: Diagnosis and treatment of tachycardias. In 2000 Yearbook of They pointed out that magnesium is safe and easy to use Intensive Care and Emergency Medicine. Edited by Vincent JL. Berlin– and should be available for immediate use in all inten- Heidelberg–New York: Springer; 2000:638–648. sive care units and emergency departments [41]. 2 Trappe HJ, Schuster HP: Clinical findings and surface ECG in emergency decision making. In Die Notfalltherapie bei akuten Herzrhythmusstörungen. Edited by Trappe HJ, Schuster HP. Darmstadt: Steinkopff-Verlag; 2001:3–14. Clinical implications 3 Trappe HJ, Rodriguez LM, Smeets JLRM, et al.: Diagnosis and therapy in Atrial fibrillation, ventricular tachycardia, and patients narrow QRS tachycardia. In Die Notfalltherapie bei akuten Herzrhyth- musstörungen. Edited by Trappe HJ, Schuster HP. Darmstadt: Steinkopff- after cardiac arrest due to ventricular fibrillation are Verlag; 2001:15–27. “classical” patients in intensive care units and emergen- 4 Trappe HJ, Rodriguez LM, Smeets JLRM, et al.: Diagnosis and therapy in wide cies. It has been shown that evaluation of history, physi- QRS tachycardia. In Die Notfalltherapie bei akuten Herzrhythmusstörungen. Edited by Trappe HJ, Schuster HP. Darmstadt: Steinkopff-Verlag; cal examination, and the 12-lead-surface electrocardio- 2001:28–39. gram are essentials for correct diagnosis and treatment. 5 Reinelt P, Karth GD, Geppert A, et al.: Incidence and type of cardiac arrhyth- In all patients with cardiac arrhythmias in intensive care mias in critically ill patients: a single center experience in a medical- and emergencies who have unstable hemodynamics, ex- cardiological ICU. Intensive Care Med 2001, 27:1466–1473. ternal DC cardioversion is the method of choice. In pa- 6 Lampert R, Ezekowitz MD: Management of arrhythmias. Clin Geriatr Med 2000, 16:593–618. tients with atrial fibrillation, there are numerous studies 7 Baine WB, Yu M, Weis KA: Trends and outcomes in the hospitalization of that analyzed outcome and recurrences after antiarrhyth- older Americans for cardiac conduction disorders or arrhythmias, 1991– mic drug treatment. However, recently published stud- 1998. J Am Geratr Soc 2001, 49:763–770. ies showed that rhythm control is not superior to rate 8 Prystowsky EN: Management of atrial fibrillation: therapeutical options and clinical decisions. Am J Cardiol 2000, 85:3D–11D. control and, therefore, a new strategy seems to be advis- 9 Knotzer H, Mayr A, Ulmer H, et al.: Tachyarrhythmias in a surgical intensive ible to treat these patients. Nevertheless, there is general care unit: a case-controlled epidemiologic study. Intensive Care Med 2000, agreement that rate control is necessary in patients with 26:908–914. atrial fibrillation and rapid ventricular response. For this 10 Reiffel JA: Drug choices in the treatment of atrial fibrillation. Am J Cardiol indication, several well-known agents have long been 2000, 85:12D–19D. available. Treatment of recurrent ventricular tachycardia, 11 Trappe HJ: Stellenwert von Antiarrhyhmika in der Behandlung von tachykarden Herzrhythmusstörungen. Internist 2002, 43:33–44. ventricular flutter, or cardiac arrest due to ventricular 12 Clemo HF, Wood MA, Gilligan DM, et al.: Intravenous amiodarone for acute fibrillation is one of the most important problems in in- heart rate control in the critically ill patients with atrial tachyarrhythmias. Am tensive care and emergencies. A fascinating idea to treat J Cardiol 1998, 81:594–598. cardiac arrest caused by ventricular fibrillation is the au- 13 Hughes M, Binning A: Intravenous amiodarone in intensive care. Time for a tomatic external defibrillation concept. First results of reappraisal? Intensive Care Med 2000, 26:1730–1739. different studies are very promising. 14 Stambler BS: Ibutilide. Cardiol Electrophysiol Rev 1998, 2:173–175. 15 Hennersdorf MG, Perings SM, Zühlke C, et al.: Conversion of recent-onset atrial fibrillation or flutter with ibutilide after amiodarone has failed. Intensive Conclusion Care Med 2002, 28:925–929. Emergency medicine and critical care are fields that of- 16. The Atrial Fibrillation Follow-up Investigation of Rhythm Management • (AFFIRM) Investigators: A comparison of rate control and rhythm control in ten require rapid diagnosis and intervention for specific patients with atrial fibrillation. N Engl J Med 2002, 347:1825–1833. This randomized, multicenter study compared two different treatment strategies in situations. It is well known that in all patients with tachy- patients with atrial fibrillation and high risk of stroke or death. The primary endpoint arrhythmias, evaluation of the underlying etiology and was overall mortality. A total of 4060 patients were enrolled in the study and ran- domized to rhythm control or rate control. The study showed that rhythm-control the degree of left ventricular function (dysfunction) is strategy offers no survival advantage over the rate-control strategy in patients with essential. Correct treatment of arrhythmias in the inten- atrial fibrillation. sive care patient is based on an understanding of the 17 Van Gelder IC, Hagens VE, Bosker HA, et al.: Crinhs HJGM for the Rate mechanism that caused the situation. The therapeutic •• Control versus Electrical Cardioversion for Persistent Atrial Fibrillation Study Group: A comparison of rate control and rhythm control in patients with re- role of antiarrhythmic drugs in the management of atrial current persistent atrial fibrillation. N Engl J Med 2002, 347:1834–1840. fibrillation or cardiac arrest is debatable. After the AFFIRM In this randomly assigned study, 522 patients with persistent atrial fibrillation were included after a previous electrical cardioversion. Patients were randomized to and RACE studies, the restoration of sinus rhythm is not rhythm control or rate control. The endpoint of this study was a composite death the goal in any patient, and rate control is an alternative from cardiovascular causes, heart failure, thromboembolic complications, bleed- ing, implantation of a pacemaker, or severe adverse effects of drugs. It was shown way for these patients. The prophylactic administration that rate control was not inferior to rhythm control. of antiarrhythmic drugs has never been studied formally 18 Delle Karth G, Geppert A, Neunteufl T, et al.: Amiodarone versus diltiazem for in victims of cardiac arrest. The optimal dose of antiar- rate control in critically ill patients with atrial tachyarrhythmias. Crit Care Med rhythmic drugs, whether best given before or only after 2001, 29:1149–1153. 19 Stambler BS, Wood MA, Ellenbogen KA, et al.: Efficacy and safety of re- multiple defibrillation shocks have failed to restore cir- peated intravenous doses of ibutilide for rapid conversion of atrial flutter or culation, is not yet known. fibrillation. Circulation 1996, 94:1613–1621. Arrhythmias in intensive care patient Trappe et al. 355

20 Ellenbogen KA, Stambler BS, Wood MA: Efficacy of intravenous ibutilide for cerebral tissue oxygen tension in a patient during cardiopulmonary resusci- rapid termination of atrial fibrillation and atrial flutter: a dose-response study. tation. Intensive Care Med 2003, 29:1016–1019. J Am Coll Cardiol 1996, 28:130–136. 32 Sefrin P: Resuscitation in emergency medical services: what factors influence 21 Volgman AS, Carberry PA, Stamber BS: Conversion efficacy and safety of the success rate? Intensivmed 2001, 38:554–560. intravenous ibutilide compared with intravenous procainamide in patients with atrial flutter or fibrillation. J Am Coll Cardiol 1998, 31:1414–1419. 33 American Heart Association in collaboration with the International Liaison Committee on Resuscitation (ILCOR): Introduction to the International guide- 22 Vos MA, Golitsyn SR, Stangl K: Superiority of ibutilide (a new class III agent) lines 2000 for cardiopulmonary resuscitation and emergency cardiovascular over DL-sotalol in converting atrial flutter and atrial fibrillation. The care—an international consensus on science. Resuscitation 2000, 46:3–15. Ibutilide/Sotalol Comparator Study Group. Heart 1998, 79:568–575. 34 Valenzuela TD, Roe DJ, Nichol G, et al.: Outcomes of rapid defibrillation by 23 Introduction to the International Guidelines 2000 for CPR and ECC: a con- security officers after cardiac arrest in casinos. N Engl J Med 2000, sensus on science. Circulation 2000, 102:1–11. 343:1206–1209. 24 Alboni P, Tomasi C, Menozzi C: Efficacy and safety of out-of-hospital self- 35 Page RL, Joglar JA, Kowal RC, et al.: Use of automated external defibrillators administered single-dose oral drug treatment in the management of infre- by a US airline. N Engl J Med 2000, 343:1210–1216. quent, well-tolerated paroxysmal supraventricular tachycardia. J Am Coll Car- diol 2001, 37:548–553. 36 Caffrey SL, Willoughby PJ, Pepe PE, et al.: Public use of automated external defibrillators. N Engl J Med 2002, 347:1242–1247. 25 Marik PE, Varon J: Cardiopulmonary resuscitation: lessons from the past and • Automatic external defibrillators save lives when they are used by designated per- trends for the future. In: 2000 Yearbook of intensive care and emergency sonnel in certain public settings. This study was performed at three Chicago air- medicine. Edited by Vincent JL. Berlin–Heidelberg–New York: Springer; ports in a prospective way during a 2-year period. It was pointed out that automatic 2000:649-657. external defibrillators deployed in readily accessible, well-marked public areas were 26 Hansen WL, Fylling F, Steen T, et al.: Delaying defibrillation to give basic used effectively to assist patients with cardiac arrest. In the cases of survivors, most cardiopulmonary resuscitation to patients with out-of-hospital ventricular fi- of the users had no duty to act and no prior training in the use of these devices. brillation: a randomised trial. JAMA 2003, 19:1389–1395. 37 Peberdy MA: Defibrillation. In Cardiology Clinics. Edited by Kern KB. Phila- 27 Lau EW: The reliable electrocardiographic diagnosis of regular broad com- delphia: WB Saunders; 2002:13–21. plex tachycardia: a holy grail that will forever elude the clinician’s grasp? Pac- ing Clin Electrophysiol 2002, 25:1756–1761. 38 Kudenchuk PJ: Advanced cardiac life support antiarrhythmic drugs. In Cardi- ology Clinics. Edited by Kern KB. Philadelphia: WB Saunders; 2002:79–87. 28 Aghababian RV, Mears G, Ornato JP, et al.: cardiac arrest management. Pre- hosp Emerg Care 2001, 5:237–246. 39 Taylor SE: Amiodarone: an emergency medicine perspective. Emerg Med 2002, 14:422–429. 29 Guidelines 2000 for cardiopulmonary resuscitation and emergency cardio- vascular care. International consensus on science. Circulation 2000; 102:1– 40 Kudenchuk PJ, Cobb LA, Copass MK, et al. Amiodarone for resuscitation 376. after out-of-hospital cardiac arrest due to ventricular fibrillation. N Engl J Med 1999, 341:871–878. 30 Bur A, Kittler H, Sterz F, et al.: Effects of bystander first aid, defibrillation and advanced life support on neurologic outcome and hospital costs in patients 41 Kaye P, O’Sullivan I: The role of magnesium in the emergency department. after ventricular fibrillation cardiac arrest. Intensive Care Med 2001, Emerg Med 2002, 19:288–291. 27:1474–1480. 42 Stuehlinger HG, Thell R, Laggner AN: Magnesium in emergency medicine. 31 Imberti R, Bellinzona G, Riccardi F, et al.: Cerebral perfusion pressure and Intensivmed 2003, 40:308–318.