Chapter 23: Arrhythmia Diagnosis and Management

Acutely ill patients frequently have significant arrhythmias. By some estimates between 12% and 19% of patients in critical care unit settings have sustained arrhythmias.^1,2 Patients following cardiac and thoracic surgery have a significant incidence of postoperative arrhythmias, specifically atrial fibrillation. Tachycardias are more common than bradycardias and atrial arrhythmias are more common than ventricular arrhythmias. Patients with underlying heart disease are more likely to have clinically significant arrhythmias. In the intensive care unit (ICU), multiple stimuli and associated elevated catecholamine levels contribute to arrhythmias. These include infection, electrolyte abnormalities, medications, ischemia, anemia, hypoxia, and changes in volume status and hemodynamics. Majority of these arrhythmias are secondary to at least one of these factors and usually respond to treatment of the primary medical or surgical processes.

Cardiac arrhythmias prolong the ICU length of stay of patients even if they are not the primary cause of their admissions and contribute to the morbidity and mortality of these patients. It is important to differentiate between those arrhythmias that need to be treated and those that are more benign so that a proper treatment plan can be instituted.

Tachycardias can be due to increased automaticity, reentry, or triggered activity. The stress seen in ICU patients can bring out or exacerbate underlying genetic or congenital predispositions, such as accessory pathways like Wolff-Parkinson-White Syndrome, Brugada syndrome, reentry arrhythmias, and congenital long QT syndromes. When assessing 12-lead electrocardiograms (EKG), monitor strips and a careful physical examination are important in addition to looking for structural heart disease.

Myocardial dysfunction, valvular abnormities, pericardial disease, congenital heart disease, and conduction abnormalities may be present. Acute cardiac dysfunction due to sepsis or related to high catecholamine states (Takotsubo syndrome) should also be considered in these critically ill patients.

The hemodynamic stability of the patient also needs to be assessed in addition to blood test analysis, medication lists, and EKG and telemetry analysis. Electrolyte abnormalities and renal or hepatic failure can be contributory. The presence of hemodynamic compromise or associated ischemia indicates the need for acute intervention. Reversible factors should be identified and treated. Significant prolongation of the QT interval is likely due to electrolyte abnormalities, such as hypomagnesemia and hypokalemia or to medications. The use of inotropes and vasopressor agents can increase heart rate (HR) and induce tachyarrhythmias. Fever, respiratory failure and severe anemia can also be contributing factors.

Increased vagal tone can slow HR and sometimes can cause delays in cardiac conduction. Medications used to control blood pressure and tachyarrhythmias can cause further delays in conduction and heart block in patients with underlying conduction system disease. Beta-blockers, calcium channel blockers, digoxin, narcotics, and antiemetics can cause bradycardia and sometimes higher degree atrioventricular (AV) block. Bradycardia rarely needs to be treated unless there is associated hemodynamic instability.

Progressive delay in conduction of intracardiac electrical impulses can occur. Isolated first-degree AV block with prolongation of the PR interval to more than 200 ms does not need treatment although it can be associated with other conduction abnormalities. Second-degree AV block occurs when not all sinus impulses are transmitted to the ventricle. In Mobitz type I (Wenckebach) second-degree AV block there is progressive lengthening of the PR interval with constant P-P intervals eventually leading to nonconducted P waves in a pattern of group beating (ratio of P waves to QRS complexes). This is usually due to a reversible delay of conduction in the AV node and is likely due to increased vagal tone or medications. It rarely needs treatment unless there is severe bradycardia and associated hypotension. Mobitz type II second-degree AV block, high-degree block, and complete heart block involve varying degrees of delay in the infranodal conduction system and are usually due to intrinsic conduction system disease. A lower ventricular escape rhythm with a rate of 25 to 40 beats/min is often present in complete heart block in an attempt to maintain cardiac output but may not provide an adequate HR (Figure 23–1a). Patients are less likely to remain hemodynamically stable with higher degrees of AV block and usually require temporary pacing with either a transthoracic or transvenous pacemaker and ultimately permanent pacing if the heart block persists. While atropine increases HR by decreasing vagal tone and the degree of AV block with type I AV block, it is usually ineffective in increasing HR with infranodal conduction delays and may actually increase the degree of block by increasing sinus rate without the ability to increase ventricular rate. Another common cause of bradycardia in the ICU occurs in patients with alternating bradycardia and tachyarrhythmias (Tachy–Brady syndrome) or paroxysmal atrial fibrillation, who have delayed sinus node recovery times either due to intrinsic conduction system disease or to the medications used to control the tachycardia. They can have prolonged pauses when they convert to sinus rhythm and may require pacing to allow adequate medication to control their arrhythmia without periods of symptomatic bradycardia.

AV dissociation occurs when there is loss of the usual pattern of atrial and ventricular synchrony and there is no association between P waves and the QRS complexes. This can be caused by heart block as discussed earlier where impulses cannot be transmitted through the AV node and a lower focus (escape rhythm) takes over (Figure 23–1a). Persistent heart block usually leads to permanent pacemaker implantation. A benign form of AV dissociation is called isoarrhythmic AV dissociation (Figure 23–2), which occurs when the sinus rate is slower than or approximately the same as a lower intrinsic cardiac rhythm so the rhythms alternate. This is commonly a junctional rhythm of 50 to 60 beats/min and does not need treatment unless there is associated hemodynamic instability. Isoarrhythmic AV dissociation resolves with an increase in the sinus rate. Acceleration of a lower focus such as a junctional or ventricular tachycardia can also cause AV dissociation. These rhythms usually require treatment if sustained or symptomatic.

ICU patients frequently have atrial and ventricular beats, which rarely need to be treated unless there is a sustained arrhythmia. Even frequent ventricular premature contractions (VPCs) with couplets, periods of bigeminy, and short runs do not need treatment unless the cardiac output is compromised. Underlying provocative causes, such as ischemia, left ventricular dysfunction, medication toxicity (eg, digoxin), or electrolyte abnormalities should be identified and addressed.

Sustained arrhythmias are less frequent but not uncommon. It is usually possible to differentiate between atrial and ventricular arrhythmias, but one of the biggest challenges in critically ill patients is to define the etiology of a wide complex tachycardia. Knowledge of the baseline EKG is important to help differentiate these arrhythmias. Patients with baseline right or left bundle branch blocks (LBBBs) have wide complex tachycardias, which are supraventricular with a QRS morphology that is the same as their baseline EKGs and are usually preceded by P waves. Some patients develop rate-related bundle branch blocks usually with an increase in HR that can cause confusion, but similarly are supraventricular, usually sinus in origin and due to variable delay in the conduction system and refractory periods of the bundle branches. Another form of wide complex supraventricular tachycardia can occur in patients with preexcitation syndromes when there is orthodromic conduction down the accessory pathway. These forms of supraventricular tachycardias need to be differentiated from ventricular rhythms.

The morphology of the QRS complexes can help differentiate supraventricular from ventricular rhythms. Ventricular tachycardias, while more likely to have LBBB configurations, have varying conduction patterns, have longer QRS durations (> 0.14-0.16 ms) and have greater leftward axis deviation. Evidence of AV dissociation with fusion or capture beats usually indicates a lower origin of the arrhythmia such as ventricular tachycardia.

Atrial fibrillation, atrial flutter, AV nodal reentry tachycardia, ectopic atrial tachycardia with rapid ventricular rates, and underlying preexcitation with an atrial arrhythmia form the majority of atrial tachyarrhythmias that manifest in the critically ill patient. Figure 23–3 lays out a classification scheme for narrow complex supraventricular tachycardias based on the regularity of the rhythm.

Initial evaluation is directed toward assessing hemodynamic stability. In the setting of hemodynamic compromise (eg, symptomatic hypotension, angina, heart failure, or myocardial ischemia) urgent electrical cardioversion is indicated. The major goal of acute treatment is to slow the ventricular rate so as to restore hemodynamic stability by improving cardiac output and blood pressure. For patients that are hemodynamically stable, initial rate control strategy should be considered. Further treatment is directed toward eliminating or reversing the precipitating or exacerbating causes. Correction of alkalosis, hypokalemia, hypomagnesemia, and hypoxemia will increase the likelihood of rate control and eventual conversion to or maintenance of sinus rhythm.

About 65% of regular supraventricular tachycardias are due to atrioventricular nodal reentrant tachycardia (AVNRT).³ AV nodal reentrant tachycardias are rhythm disturbances that depend on the properties of the AV node for initiation and propagation. In a typical circuit, activation proceeds down the anterograde “slow” pathway and returns via the retrograde “fast” pathway. The arrhythmia results from an endless circle of electrical impulses conducted down one pathway and up another with slow and fast pathways cooperating to facilitate and maintain the circuit. The atypical form of AVNRT involves antegrade conduction down the “fast” perinodal pathway and retrograde conduction via the “slow” perinodal pathway. AV nodal reentrant tachycardias usually have ventricular rates of 150 to 220 beats/min, but can be as fast as 250 beats/min. AV conduction is usually 1:1, but rarely 2:1. It usually begins with a premature atrial depolarization. There can be a pseudo R' in lead V1, a pseudo-S wave in the inferior leads and retrograde P wave can be seen in other leads. If the initial diagnosis is unclear, adenosine (6-12-12 mg intravenously) usually will break the reentry circuit and restore sinus rhythm (Figure 23–4). A brief intervening period of sinus bradycardia or complete heart block may occur. With atrial tachycardia, atrial flutter, or atrial fibrillation, increasing AV block with adenosine will usually make the diagnosis apparent while with sinus tachycardia the heart will slow gradually in response to adenosine and then return to the pretreatment rate.

For the hemodynamically unstable or symptomatic patient with AVNRT, initial choices include adenosine or direct current (DC) cardioversion to restore sinus rhythm and hemodynamic stability. Adenosine has a rapid onset and an extremely short half-life, making it the drug of choice for acute treatment of narrow complex tachyarrhythmias, but it is not useful in preventing recurrences.

For the hemodynamically stable patient, treatment approaches include vagal maneuvers (eg, Valsalva maneuver or carotid sinus massage), adenosine, nondihydropyridine calcium channel blockers (eg, verapamil 5 mg IV bolus or diltiazem 0.25 mg/kg infusion given over 2 minutes) and beta-blockers (eg, metoprolol with 5 mg boluses or esmolol, 0.5-1.0 mg/m² bolus). These drugs alter conduction velocity through the AV node (see Figure 23–4). Calcium channel blockers and beta-blockers decrease the likelihood of recurrence and should be considered in patients with early recurrent arrhythmia after administration of adenosine. Continued intravenous (IV) infusions may be needed to prevent early recurrences. For long-term management of patients with symptomatic episodes of this tachyarrhythmia, options include pharmacologic therapy and radiofrequency catheter ablation with the latter providing high curative success rates.

Atrial tachycardia is a narrow complex tachyarrhythmia with impulse generation outside of the sinus node that does not rely on accessory pathways, AV node, or ventricular tissue for generation and propagation.³ Atrial tachycardia is usually focal in origin and can arise from any ectopic focus in the left atrium, right atrium, vena cava, or pulmonary veins. The underlying mechanism can involve reentry, enhanced automaticity, or triggered activity. Atrial tachycardia may occur from atrial stretch, digitalis toxicity, electrolyte imbalance, and catecholamine excess with or without underlying cardiac disease. On the EKG, the P wave generally precedes the QRS complex; however, it has a morphology that is distinct from the sinus P wave. The P wave axis is usually abnormal and may help in localizing the site of origin of the tachycardia. AV nodal blockers and digoxin do not terminate this arrhythmia, but can be used to slow down the ventricular rate and improve hemodynamics. In select cases, there may be a role for class Ia, Ic, or III antiarrhythmic agents. Electrical cardioversion plays a limited role in the management of atrial tachycardia as the underlying pathophysiology is usually enhanced automaticity, which in most cases renders cardioversion ineffective with a high rate of arrhythmia recurrence.

Multifocal atrial tachycardia is usually associated with underlying pulmonary disease especially severe chronic obstructive lung disease or respiratory failure in older, acutely ill individuals.³ It can also occur in patients with other forms of pulmonary or cardiac disease. Electrolyte imbalance, hypoxia, acidosis, and drugs, such as isoproterenol and theophylline are also associated with this arrhythmia. It is characterized by an irregularly irregular rhythm with a ventricular rate greater than 100 beats/min and at least 3 unique P-wave morphologies each felt to indicate multiple atrial activation sites. Treatment is aimed at the underlying disease. Verapamil may be effective and sometimes slows ventricular response, but is not effective in all patients.

Atrial flutter is a macroreentrant atrial tachycardia typically involving the right atrium. It usually coexists with atrial fibrillation and is uncommon in a structurally normal heart.³ The atrial flutter rate is usually 300 beats/min, but can be slower (240-440 beats/min) especially in patients on antiarrhythmic therapy. The ventricular rate which is determined by the AV conduction ratio is usually a 2:1 with the resultant ventricular rate of approximately 150 beats/min (Figure 23–5). Higher degrees of AV block and variable HRs can be seen in patients due to underlying cardiac disease or AV nodal conduction disease and those on antiarrhythmic agents. Atrial flutter with 1:1 AV conduction and ventricular rates as high as 300 beats/min is poorly tolerated and can be seen in cases of sympathetic stimulation or in the presence of an accessory pathway. Flutter waves are best identified in the inferior leads and demonstrate a typical “sawtooth pattern” with absence of an isoelectric baseline. The flutter waves are negative in the inferior leads if the reentry circuit is anticlockwise and positive if the reentry circuit is clockwise (uncommon variant). The rhythm while usually regularly can be irregular in the presence of variable AV block.

In patients with acute hemodynamic collapse or severe symptoms due to atrial flutter, DC synchronized cardioversion is indicated. Atrial flutter can be converted using relatively small amounts of electrical energy, usually less than 50 joules. Alternatively, if pharmacologic conversion is deemed necessary, ibutilide is considered the drug of choice, but carries a risk of QT prolongation and torsade de pointes mandating close monitoring with aggressive repletion of magnesium and potassium.

Atrial flutter also can be converted to sinus rhythm with overdrive pacing. Atrial flutter is amenable to radiofrequency ablation, with success rates approaching those for other supraventricular tachycardias and provides effective long-term treatment. AV nodal blockers can be used to slow down the ventricular rate in hemodynamically stable patients; however, rate control is more difficult to achieve in atrial flutter. Digoxin can be considered for ventricular rate control in patients with congestive heart failure or hypotension.

Regardless of whether a rate or rhythm control method is employed, anticoagulation strategies to prevent systemic embolization must be considered in patients with atrial flutter. The risk assessment and therapeutic recommendations follow the same principal as atrial fibrillation.

Atrial fibrillation is the most common dysrhythmia in the general population and is highly prevalent in the critically ill.⁴ Affected patients are at increased risk of cardiovascular morbidity and mortality.⁵ It is characterized by disorganized atrial electrical activity probably owing to multiple reentry circuits within the atria that results in loss of atrial contraction and irregular and often times rapid ventricular rates. It is easily recognized on the surface EKG as a narrow complex, irregularly irregular, supraventricular rhythm with a loss of clear P waves, and/or the presence of fibrillatory waves (Figure 23–6). This feature distinguishes atrial fibrillation from the other organized atrial arrhythmias.

Atrial fibrillation increases with age and is greater in men compared to women. Most forms of structural heart disease are associated with atrial fibrillation; most commonly hypertensive heart disease, underlying coronary artery disease, and rheumatic heart disease. Other cardiopulmonary and systemic diseases including obstructive sleep apnea, diabetes, obesity, metabolic syndrome, hyperthyroidism, chronic kidney disease, and postsurgical states have also been associated with atrial fibrillation. Premature atrial contractions are a trigger for atrial fibrillation. In addition, transition between atrial fibrillation and other supraventricular arrhythmias, especially typical atrial flutter is noted frequently. Initial diagnostic workup should include a careful history and physical examination(focusing on the duration and symptoms associated with the arrhythmia, identifiable exacerbating factors, and underlying cardiopulmonary or systemic disease processes), pertinent labs (including serum electrolytes and thyroid function tests), and specific cardiovascular workup (transthoracic and in select cases transesophageal echocardiogram).

As with other arrhythmias, initial assessment should focus on hemodynamic stability as well as identification and correction of underlying causes. Therapeutic considerations in atrial fibrillation include the three nonmutually exclusive strategies of rate control, rhythm control, and systemic thromboembolism prevention.^6,7,8,9 Recent clinical trials have demonstrated similar outcomes with rate and rhythm control strategies; however, there may be crossover from one to another strategy due to the natural history of the disease, failure of the initial strategy, or patient preference.¹⁰

Rhythm control strategies include synchronized DC cardioversion, pharmacologic conversion using antiarrhythmic drugs, radiofrequency catheter ablation, and/or surgical procedures (eg, Maze procedure). Urgent cardioversion should be considered for hemodynamically unstable, severely symptomatic patients, and in the presence of underlying preexcitation. Indications have been summarized in Table 23–1. Several antiarrhythmic agents can be used for pharmacologic rhythm control; however, careful attention should be paid to appropriate patient selection and the side-effect profile and proarrhythmic potential of these medications.

For patients without evidence of structural heart disease or coronary artery disease, class Ic agents like propafenone or flecainide can be considered. Patients should be monitored for QRS widening after initiation of these drugs. For patients with evidence of structural heart disease, amiodarone, sotalol, dronedarone, ibutilide, and dofetilide are the most commonly recommended antiarrhythmic agents. In patients with coronary artery disease without left ventricular dysfunction sotalol, dofetilide, amiodarone, and dronedarone are reasonable choices. In patients with left ventricular (LV) dysfunction and clinical heart failure, antiarrhythmic choices include amiodarone and dofetilide. QT interval should be monitored with class III antiarrhythmics. Sotalol and dofetilide are both affected by renal insufficiency and may require dose adjustment or discontinuation. Amiodarone requires dose adjustment in hepatic dysfunction and has significant systemic side effects with a propensity to cause pulmonary, cardiac, thyroid, ocular, dermatologic, hepatic, and gastrointestinal side effects which must be carefully considered prior to initiating treatment.

Most patients will require slowing of the ventricular rate associated with atrial fibrillation. Pharmacologic approach includes AV nodal blocking agents, namely, nondihydropyridine calcium channel blockers and beta-blockers. In patients with congestive heart failure or hypotension, digoxin can be considered. In select patients, combination therapy may be necessary, but excessive AV nodal blockade should be avoided. A-V node ablation with ventricular pacing is an alternative nonpharmacologic rate control approach, but rarely an acute treatment.

An important aspect of atrial fibrillation management includes prevention of thromboembolism. Patients with atrial fibrillation are at risk for systemic embolization and stroke. The noncontracting atria are a potential nidus for thrombus formation, which usually occurs in the left atrium and left atrial appendage. Multivariate risk models are available to aid in estimation of the thromboembolic risk in patients with nonvalvular atrial fibrillation so that appropriate antithrombotic prevention strategies can be recommended. The most commonly used and well validated being the CHADS2 point score (Congestive heart failure, Hypertension, Age ≥ 75 years, Diabetes mellitus, and prior Stroke or transient ischemic attack) index.¹¹ Patients without any of these risk factors have a CHADS2 score of 0 are at low risk of thromboembolic events and do not require long-term antithrombotic therapy. Patients with a score of 1 are at intermediate risk and can be treated with oral anticoagulant therapy or aspirin. Patients with a score of 2 or higher on the CHADS2 index are considered to be at high risk for thromboembolic events and anticoagulant therapy is recommended unless there are contraindications. Choices include the conventionally used vitamin K antagonist warfarin or newer direct thrombin inhibitor such as dabigatran and factor Xa inhibitors, such as rivaroxaban or apixaban. The new agents should not be used in the presence of severe renal insufficiency, prosthetic heart valves, and in cases of valvular atrial fibrillation. Initial therapy in critically ill patients may be unfractionated or fractionated heparin in the acute period of care prior to conversion to one of these agents.

Hemodynamically stable patients with atrial fibrillation of unknown duration or those with atrial fibrillation for more than 48 hours should be therapeutically anticoagulated for 3 to 4 weeks before elective conversion is attempted. Alternatively, the patient can be started on anticoagulation and if a transesophageal echocardiogram rules out existing thrombi, elective cardioversion can be performed safely. Anticoagulation should be continued for 4 weeks after cardioversion.

The differences in the pathophysiology and management of patients that present with atrial fibrillation with an underlying accessory pathway are noteworthy. A rapid ventricular rate (usually greater than 200 beats/min) and evidence of preexcitation are clues to this diagnosis. For hemodynamically unstable patients urgent cardioversion should be considered. AV nodal blockers should be avoided as they can promote conduction down the accessory pathway resulting in rapid ventricular rates and ventricular fibrillation. Digoxin and adenosine should also be avoided. Antiarrhythmic choices for rhythm control include procainamide, amiodarone, ibutilide, flecainide, and propafenone. Transvenous radiofrequency catheter ablation of bypass tracts obviates the need for long-term pharmacologic therapy and has largely replaced surgical ablation due to its high curative success rates in patients with bypass tracts.

Ventricular tachycardia is defined as 3 or more consecutive VPCs at a rate of at least 100 beats/min, but is not considered sustained unless it is persists for at least 30 seconds. It is usually monomorphic and is a reentry arrhythmia (Figure 1b). This is easily differentiated from an accelerated idioventricular rhythm (AIVR) which is a wide complex rhythm at 40 to 60 beats/min that is usually due to increased automaticity or is an escape rhythm due to bradycardia (Figure 1a). AIVR is usually transient and does not require treatment other than addressing the underlying cause. Rapid ventricular tachyarrhythmias, especially in patients with structural heart disease and ischemia are more likely to cause hemodynamic compromise and to degenerate into ventricular fibrillation. Ventricular fibrillation requires emergency defibrillation as per Advanced Cardiac Life Support recommendations and protocols.¹² Unstable patients such as those with hypotension, exacerbation of heart failure, obtundation, or unstable ischemic chest pain who develop ventricular tachycardia should be treated by emergency electrical cardioversion starting with 100 to 200 J and increasing up to 360 J to restore sinus rhythm. Pharmacologic treatment may be needed in addition, but can be used alone in patients who have sustained ventricular tachycardia and remain hemodynamically stable.¹³ These drugs need to be used carefully as many antiarrhythmic agents have significant proarrhythmic side effects and potassium and magnesium replacement should be given. Initial treatment with amiodarone is recommended as a first-line agent. IV infusion of 150 mg of amiodarone over 10 minutes can be given. The full loading dose of amiodarone is given over 24 hours at 1 mg/min over the first 6 hours followed by 0.5 mg/min over the next 18 hours for a total of 1050 mg. Subsequent maintenance doses can be given orally or intravenously as tolerated. Beta-blockers and procainamide are alternatives. Lidocaine can be used in patients with acute cardiac syndromes and other drugs, such as sotalol, propafenone, and flecainide are second-line agents due to their high incidence of proarrhythmic effects. Overdrive pacing can be considered in patients with sustained ventricular arrhythmias that are refractory to antiarrhythmic agents.

Torsade de pointes and other forms of polymorphic tachycardia are rapid ventricular rhythms associated with hemodynamic instability and a predisposition to degenerate into ventricular fibrillation.¹⁴ Polymorphic ventricular tachycardia is commonly associated with ischemia and is likely to require cardioversion and consideration of rapid myocardial revascularization. In Torsades de pointes, the morphology of the QRS complexes varies in a pattern of twisting points and changes of axis associated with marked QT prolongation of greater than 500 ms (Figure 23–7). It can be caused by electrolyte abnormalities, ischemia, and proarrhythmic effects of antiarrhythmic agents such as flecainide, propafenone, quinidine, and sotalol and by other agents and drug interactions that increase the QT interval. Common causative agents include antibiotics, antihistamines, antifungal agents, tricyclic antidepressants, and phenothiazines. Although less common than acquired QT prolongation are patients with congenital QT prolongation (Romano–Ward Syndrome and Lange–Jervell–Neilson Syndrome) who are at risk for polymorphic ventricular tachycardia. Treatment is directed to reversing the inciting causes of the arrhythmia and to shortening the QT interval. IV magnesium should be given and potassium level repleted to 4.5 to 5 mmol/L. The stimulating factors should be removed or corrected as much as possible. The absolute QT interval should be shortened by increasing the HR with atropine, isoproterenol infusion, or overdrive pacing. As with any unstable patient with ventricular tachycardia, electrical cardioversion may be needed.

Other less common causes of ventricular tachycardia/ventricular fibrillation can sometimes be found in patients in the ICU and need to be recognized. Patients with Brugada syndrome may be predisposed to polymorphic ventricular tachycardia and ventricular fibrillation. EKGs show varying degrees of right bundle branch block and right precordial ST elevations, which may not always be present at baseline, but can be induced during periods of stress and by medications. These patients with life threatening arrhythmias will require automatic implantable cardioverter defibrillator (AICD) implantation in addition to the acute treatment described earlier. Another variant of stress or exercise-induced ventricular tachycardia usually arises from the right ventricular outflow tract and less commonly from a site in the left ventricular outflow tract. This is usually a more benign arrhythmia that presents with paroxysmal ventricular tachycardia with a LBBB pattern that responds to adenosine or beta-blockers. This rhythm can eventually be treated with radiofrequency catheter ablation of the initiating site in the outflow tract although long-term treatment with beta-blockers can be effective.

All ventricular arrhythmias can be markers for poorer long-term prognosis and sudden death in patients associated with left ventricular dysfunction and ischemic heart disease.¹³ Patients with nonsustained ventricular tachycardias and ischemic heart disease in ICU settings, especially those with acute cardiac syndromes should be given beta-blockers to control HR, blood pressure, and rhythm disturbances in addition to electrolyte replacement and control of other stimulatory factors such as anemia, pain, and fever. Long-term treatment strategies for these patients may include AICDs and biventricular pacing especially if there is persistent left ventricular dysfunction with no reversible inciting factors for the ventricular arrhythmia. While these devices have improved outcome in some patients, they are rarely indicated acutely in the treatment of patients in the ICU. Patients should eventually be referred for cardiac evaluation to see if they qualify for device implantation under the current guidelines.^13,15,16 Patients with ventricular arrhythmias and structural heart disease, such as hypertrophic cardiomyopathies and congenital syndromes, such as Brugada syndrome may benefit from earlier electrophysiologic referral for secondary prevention of ventricular arrhythmias and sudden death.