Tachycardia and Bradycardia

7 Tachycardia and Bradycardia

Cardiac arrhythmias, a common problem encountered in the intensive care unit (ICU), increase the length of stay and represent a major source of morbidity.¹ Clinical issues such as electrolyte derangements (particularly those related to potassium and magnesium ion concentrations), acidemia, hypoxia, cardiac ischemia or structural defects, and catecholamine excess (exogenous or endogenous) can play important roles in the cause of arrhythmias. Treatment of these arrhythmias depends most importantly on the cardiac physiology of the patient but also on the ventricular response rate and duration of the arrhythmia.

The two major categories of cardiac arrhythmias are defined by heart rate: bradycardia (heart rate <60 beats per minute [bpm]) and tachycardia (heart rate >100 bpm). Asymptomatic bradycardia does not carry a poor prognosis, and in general no therapy is indicated.² Bradycardia with or without hypotension should prompt a consideration of metabolic disturbances, hypoxemia, drug effects, and myocardial ischemia. Other causes of bradycardia are shown in Table 7-1.

TABLE 7-1 Common Causes of Bradycardia

Medications that can cause bradycardia include β-adrenergic blockers, Ca⁺ channel blockers, clonidine, antiarrhythmics, digoxin, and propofol. Severe toxicity due to overdose with a β-adrenergic antagonist (leading to bradycardia, hypotension, shock) can be treated with glucagon (5 to 10 mg IV, followed by an infusion of 1 to 10 mg/h diluted in D₅W). Moderate drug-induced bradycardia (heart rate >40 bpm) can be observed until the offending drug is metabolized, so long as peripheral perfusion appears to be adequate. β-Adrenergic agonists, such as dopamine (3 µg/kg/min and titrated upward as needed), dobutamine, isoproterenol (2 µg/min and titrated upward as needed to increase heart rate and perfusion), or epinephrine, can be used to provide temporary support for bradycardic hypotensive patients. Bradycardia in the setting of preexisting shock and refractory acidosis is an ominous sign, and transcutaneous or transvenous pacing is generally futile.

The first step in evaluating the critically ill patient with tachycardia is to assess hemodynamic stability. It is critical to differentiate hypotension leading to tachycardia from hypotension caused by tachycardia. Examples of hypotension leading to tachycardia are the normal compensatory response to hypovolemic shock or atrial fibrillation with rapid ventricular response due to infusion of large doses of an arrhythmogenic agent (e.g., dopamine) to treat septic shock. An example of hypotension caused by tachycardia is the response to ventricular tachycardia (VT) after myocardial infarction (MI). In the former situation, intravascular volume loading or decreasing the dose of a β-adrenergic agonist is indicated. In the latter circumstance, rapid conversion by electrical cardioversion should be performed unless pharmacologic treatment is immediately successful.

Sinus tachycardia is probably the most common dysrhythmia encountered in the ICU and often occurs as a response to a sympathetic stimulus (e.g., hypoxia, vasopressors, inotropes, pain, dehydration, or hyperthyroidism). The first step is to review the patient’s medication list, including infusions, to exclude an iatrogenic etiology for the tachycardia. Treatment focuses on identifying and trying to correct the underlying cause. In trauma and postsurgical patients, tachycardia can be a sign of bleeding and hypovolemia. It is usually reasonable to administer an intravascular volume challenge (e.g., 500 mL of colloid solution in adults) and check the hemoglobin concentration. Sinus tachycardia and hypertension can be manifestations of opioid withdrawal, failure of a ventilator weaning trial, or inadequate sedation. Most patients at high risk for coronary disease warrant prophylactic treatment with a β-adrenergic blocker to prevent myocardial ischemia secondary to a high “rate-pressure product” and high myocardial oxygen demand.^4,⁵ In particular, perioperative patients with significant cardiac risk should have titrated therapy with a β-adrenergic blocker to maintain the heart rate at less than 80 bpm unless significant contraindications exist.⁶

Sustained regular tachycardia (heart rate >160 bpm) associated with a narrow QRS complex on the ECG often has a reentrant mechanism as the etiology. Reentrant narrow complex tachycardia is more prevalent in females and usually is not associated with structural heart disease. The key treatment is to block AV conduction.¹ These dysrhythmias can often be converted with carotid sinus massage. Adenosine can be administered (6 mg IV, followed by 12 mg IV if no response to the lower dose) if sequential carotid sinus massage fails to abort the dysrhythmia or is contraindicated. Patients presenting with reentrant supraventricular tachycardia in the ICU often have a past history of this dysrhythmia. β-Adrenergic blockers or calcium channel blockers are reasonable choices for both acute conversion and maintenance therapy. Specific β-adrenergic blockers include metoprolol (5 mg IV every 5 minutes until therapeutic effect is achieved) or esmolol (loading dose of 500 µg/kg over 1 minute, then 50 µg/kg/min infusion). Esmolol can be rebolused (500 µg/kg and the drip titrated to a maximum of 400 µg/kg/min). For diltiazem, use 5- or 10-mg boluses, using higher doses only after it is determined that administration of the agent does not lead to arterial hypotension.

The prevalence of atrial fibrillation (AF) in the general population increases exponentially with age, from 0.9% at 40 years to 5.9% in those older than 65.⁷ The most important risk factors for development of AF in the general population are structural heart disease (70% in the Framingham study⁸ over a 22-year follow-up), hypertension (50%),⁸ valvular heart disease (34%),⁹ and left ventricular hypertrophy. AF should be approached in the following manner: find the cause and try to fix it; if the underlying problem is not fixable, consider rate control and anticoagulation. AF with rapid ventricular response can cause significant hemodynamic instability requiring emergent electrical cardioversion (biphasic defibrillator). The initial attempt should be synchronized, using 50 J of energy. If unsuccessful, subsequent cardioversion attempts should use escalating energy levels (e.g., 100, 120, 150, 200 J). AF with rapid ventricular response in the absence of hemodynamic instability can be managed initially by using drugs or other interventions to provide rate control. The goal should be to reduce heart rate to less than 120 bpm. First, minimize adrenergic stimulation by instituting mechanical ventilation if high work of breathing and respiratory failure appear to be contributing factors. Reduce the rate of catecholamine (epinephrine, dobutamine, and/or dopamine) infusions if possible. If the patient is not currently receiving treatment with inotropes or vasopressors, consider β-adrenergic blockade as first-line therapy. Metoprolol (5 mg IV every 5 minutes) or esmolol (500 µg/kg over 1 minute, then 50 µg/kg/min infusion) are reasonable choices. A trial of diltiazem (5 to 10 mg IV bolus, followed by an infusion of 5 to 20 mg/h) also can be used. If the patient requires treatment with β-adrenergic inotropic agents to support cardiac output, amiodarone (150 mg IV bolus, followed by an infusion of 1 mg/min for 6 hours, followed by an infusion 0.5 mg/min) is a reasonable choice for both rate control and conversion therapy. Amiodarone can cause lung toxicity, even with short-term therapy, so caution is warranted when using this drug, particularly in critically ill patients with underlying lung pathology.¹⁰ Digoxin is the least effective option acutely; it is relatively ineffective for controlling ventricular rate when endogenous or exogenous adrenergic tone is high.¹¹ With new-onset AF, conversion to sinus rhythm is desirable, especially for patients who are poor candidates for anticoagulation. Conversion to sinus rhythm is also beneficial for patients with profound left ventricular dysfunction, because coordinated atrial contraction can contribute substantially to cardiac output under these conditions. In other patients, the primary goal should be to achieve (ventricular) rate control.^12,¹³ Conversion is significantly more likely to occur during rate control with β-adrenergic blockers (e.g., esmolol) than diltiazem, but this observation actually may reflect a reduction in the spontaneous conversion rate when diltiazem is used.^14,¹⁵ Amiodarone, particularly in patients with impaired ventricular function, is generally the drug of choice to achieve conversion. Anticoagulation with IV heparin should be considered if AF persists for more than 48 hours. The stroke risk in unanticoagulated patients is approximately 2% per year (0.05% per day).

Regular narrow-complex tachycardia with a heart rate between 145 and 155 bpm is typically due to atrial flutter. Carotid sinus massage or adenosine can unmask this diagnosis if it is in doubt after inspection of the 12-lead ECG (Figure 7-1). Ventricular rate control is difficult to achieve pharmacologically when the dysrhythmia is atrial flutter; accordingly, conversion to sinus rhythm is the goal. Synchronized cardioversion should be tried starting at 50 J, using appropriate conscious sedation. If cardioversion converts the rhythm to AF, use synchronized electrical cardioversion again, starting with 100 J. If atrial fibrillation persists, treat with a rate-controlling agent and anticoagulation. If refractory or recurrent atrial flutter is the problem, attempt rate control with β-adrenergic blockers or diltiazem, as for AF.