Arrhythmias in the ICU — Comprehensive Review

• Patients admitted to the intensive care unit (ICU) are at increased risk for cardiac arrhythmias.
• Cardiac arrhythmias are common in the ICU, and can be either the initial reason for admission to the ICU or a consequence of the medical condition.
• Exacerbating and contributing factors are multiple, and management of the patient requires a careful determination of these factors and correction where possible.

Patients admitted to the intensive care unit (ICU) are at increased risk for cardiac arrhythmias, which may be either the primary reason for ICU admission or a contingency in the critically ill patient. This article addresses the occurrence of arrhythmias in the critically ill patient, and their pathophysiology, implications, recognition, and management.

Although patients can be admitted to the ICU with a variety of conditions, the critical nature of their underlying processes and the supportive measures used to treat them can contribute to an elevated catecholamine state. Coupled with fluctuations in intravascular volume, electrolyte disturbances, and other metabolic derangements, this places patients at risk for cardiac arrhythmias. The incidence of arrhythmia in the ICU patient can approach 40%, most typically associated with conditions such as septic shock and respiratory failure.

1 The most common arrhythmias in the ICU setting can be divided into 2 basic categories: (1) tachyarrhythmias (eg, atrial fibrillation [AF] and atrial flutter, ventricular arrhythmias, and other supraventricular tachycardias [SVTs]) and (2) bradyarrhythmias (eg, junctional rhythm, sinus bradycardia, and atrioventricular [AV] conduction block). Predictors of tachyarrhythmia occurrence in ICU patients include the use of stimulant drugs such as norepinephrine, and a high APACHE II score (25) (see the article on Cardiogenic Shock by Shah and colleagues elsewhere in this issue). For those with bradyarrhythmias, identified predictors include the use of norepinephrine (which is a predictor of both tachyarrhythmia and bradycardia), arterial pH less than 7.

3, and HCO3 level of 18 mEq/L or higher (see Box 1 for common risk factors). 1

The presence of arrhythmia, especially ventricular fibrillation (VF), symptomatic sinus bradycardia, and junctional bradycardia, in the medical ICU has been associated with higher in-hospital mortality. Tongyoo and colleagues1 reported on a single-center population of 247 ICU patients (mean age 58. 5 years; mean APACHE II score 20. 1). In this group of critically ill patients, arrhythmias were seen in 39. 7%. The mortality among patients who developed arrhythmias was significantly higher than among those who did not. Among those who developed significant bradyarrhythmias (sinus or junctional) the mortality was 88. 7%, and in those with tachyarrhythmias (particularly VF) the mortality was 66. 7%, compared with 18. 1% mortality (P<.

001) in patients free of arrhythmias. Similar results were seen by Annane and colleagues2 among 1341 medical ICU patients, sustained arrhythmias being seen in 12% of patients. In this population, inhospital death rates were 17% in patients without arrhythmia; 29% in patients with supraventricular arrhythmia (SVA); 73% in patients with ventricular arrhythmia (VA); and 60% in patients with conduction abnormalities. The occurrence of arrhythmias in the ICU population can be associated with a prolonged stay in hospital. 3 Polanczyk and colleagues3 reported on 4181 patients aged 50 years or older who presented in sinus rhythm and underwent nonemergency, noncardiac procedures. In this group of patients, perioperative SVAs were seen in in 317 patients (7.

6%). Independent preoperative correlates for the occurrence of these arrhythmias included male sex, age 70 years or older, history of valvular heart disease or heart failure, and prior history of SVA or asthma. The occurrence of SVA was associated with a 33% increase in length of stay after adjustment for other clinical data (P<. 001). Goodman and colleagues4 reported on both short-term and long-term consequences of arrhythmias in the ICU population. This study included 611 patients Box 1 Risk factors for arrhythmia in the intensive care unit

• Male gender
• Age greater than 70 years
• Cardiac disease (coronary artery disease, heart failure, valvular disease)
• Pulmonary disease (asthma)
• Thyroid disease
• Critically ill (APACHE score 25)
• Volume fluctuations
• Electrolyte disturbances
• Metabolic derangements
• Vasopressors Managing Arrhythmias in the ICU admitted to the general ICU who were evaluated for the development of SVA. Patients were followed through hospital discharge, and 48-month mortality was evaluated. New-onset SVA was found in 9% of patients, and preexisting history of SVA in 12%. In-hospital mortalities were 18% in those with no SVA, 56% in the new-onset SVA group, and 32% in those with prior histories of SVA (P<.05 for any SVA vs no SVA; P<.05 for history SVA vs new-onset SVA). Similarly to other studies, mortality was associated with high APACHE II scores, sepsis, acute renal failure, and myocardial ischemia. For those with new-onset SVA the APACHE II score was 23.8  8 versus 16  8 for those without SVA (P<.05).4 Of note, for those surviving to discharge the postdischarge mortality rates were 20% in the no-SVA group, 36% in the newonset SVA group, and 45% in the history of SVA group (P<.05 for any SVA vs no SVA; P<.05 for history SVA vs new-onset SVA). Most deaths in the new-onset SVA group occurred during the acute hospital stay and were typically associated with multiorgan system failure as reflected in the APACHE II scores.4 Moreover, in this study new-onset SVAs were not found to be associated with a preadmission history of cardiac disease, being more closely associated with a history of underlying pulmonary disease and hypothyroidism.

Determine Urgency As in any other patient population, the management of arrhythmias in the ICU patient is determined by the acuity of the problem (Box 2). An initial critical step is determining whether an arrhythmia truly exists, or if an artifact is recorded as a result of electrical interference created by devices in the patient environment, or is created by motion (Fig. 1). If an arrhythmia is confirmed, the urgency of treatment will depend on a determination of whether the rhythm itself is causing compromise to the patient. Management will be more urgent in the setting of an acute arrhythmia that is resulting in symptomatic hypotension and/or hypoperfusion to vital organs.

Identify Causes Regardless of whether urgent steps are required, identification of correctable underlying causes should be undertaken when the patient is sufficiently stabilized (Box 3). Multiple electrolytes and acid-base abnormalities are common in the ICU patient population, and in one study were reported in around 67% of patients. 5 Hypokalemia is a well-recognized contributor to cardiac arrhythmia, and in the population with ischemic heart disease the likelihood of VF as almost twice as high among patients with potassium levels of less than 3. 6 mEq/L as in those with higher levels (odds ratio 1. 97).

6,7 In up to 40% of patients with hypokalemia there is concomitant hypomagnesemia, and unless this is corrected it may not be possible to correct the potassium level. 8 Box 2 Determinants of urgency

• Hypotension
• Ischemia
• Heart failure
• Altered mentation
• Other signs of hypoperfusion: hypoxia, decreased urine output Tracy & Boushahri Fig. 1. Telemetry strip demonstrating artifact initially thought to be ventricular tachycardia. Close examination reveals underlying sinus rhythm with motion artifact (arrows indicate QRS complexes). The relation between potentially life-threatening arrhythmias and inappropriate ventilation, hypoxemia, hypo- or hyperventilation, and metabolic acidosis has long been appreciated.9 Patients in the ICU are at risk for these potentially reversible causes of arrhythmias. Critically ill patients are with volume overload can be arrhythmogenic because of atrial stretch.10 In patients with an indwelling catheter such as a peripherally inserted central catheter or other central line, mechanical stimulation may lead to arrhythmias. Advanced Cardiac Life Support (ACLS) guidelines emphasize the “5 H” and “5 T” reversible causes of arrhythmias applicable in all clinical scenarios: Thrombosis, pulmonary/cardiac; Tension pneumothorax; Tamponade, cardiac; Trauma; Toxins; and Hypoxia; Hydrogen ions (acidosis); Hypothermia; Hypovolemia; Hypo-/Hyperkalemia.11 Care should be taken in the ICU patient to prevent or correct these potential Box 3 Causes of arrhythmia
• Hypoxia/hypoventilation
• Hypovolemia/hypervolemia
• Electrolyte imbalances (potassium, magnesium)
• Metabolic acidosis
• Hypothermia
• Coronary ischemia
• Cardiac tamponade
• Acute pulmonary process (pulmonary embolism, pneumothorax)
• Trauma
• Intoxication
• Mechanical stimulation (central line) Managing Arrhythmias in the ICU causes and contributors to arrhythmias. Without correction, management of the arrhythmia may not be possible.

An understanding of the basic mechanisms of cardiac arrhythmias is helpful in determining correct therapeutic approaches.

Bradyarrhythmias

Bradyarrhythmias (Table 1) arise from problems in impulse generation (automaticity) and/or impulse conduction (heart block). Diminished automaticity in the sinus node results in sinus bradycardia, and in more extreme cases sinus pauses. Heart block is usually due to disease (more commonly fibrosis, less commonly ischemia) in the AV node or His-Purkinje system, the latter being associated with higher grades of AV block.

The degree of heart block is determined by the extent of impulse conduction from the atria to the ventricles: in first-degree heart block all impulses are conducted, albeit at a slower rate (prolonged PR interval); in second-degree heart block they are intermittently conducted; and in third-degree heart block none of the atrial impulses are conducted.

Bradyarrhythmias can be seen in a variety of settings in the ICU, such as with elevated intracranial pressure, exaggerated vagal activity (coughing, vomiting), carotid sinus pressure (tight collar), hypothyroidism, hypothermia, ischemia, metabolic abnormalities (hyperkalemia), and various drugs (b-blockers, calcium-channel blockers, antiarrhythmics, digoxin, clonidine, opioids, lithium, dexmedetomidine). 12

Tachyarrhythmias

Tachyarrhythmias (Table 2) have 3 general mechanisms: increased automaticity, reentry, and triggered activity. Enhanced automaticity can occur in the atrium, AV node, or within the ventricle. These automatic foci in the atria, AV junction, or ventricles can accelerate and drive an ectopic tachyarrhythmia, such as paroxysmal atrial tachycardia. Automatic tachyarrhythmias (both atrial and ventricular) are commonly encountered in the ICU, as they are triggered by metabolic disturbances such as electrolyte abnormalities (namely potassium and magnesium disturbances), acid-base disturbances, hypoxemia, and ischemia. Use of vasopressors and inotropes can also contribute, given their sympathomimetic properties.

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