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  1. Sinus bradycardia is a sinus node–driven heart rate of less than 60 beats/min. Unless there is severe underlying heart disease, hemodynamic changes are minimal. With very slow rates, atrial and ventricular ectopic escape beats or rhythms may occur.
    1. Etiologies:
      1. Hypoxia.
      2. Intrinsic cardiac disease such as sick sinus syndrome or acute MI (particularly inferior wall MI).
      3. Medications such as succinylcholine (especially in young children via a direct cholinergic effect), anticholinesterases, β-adrenergic blockers, calcium channel blockers, digoxin, and synthetic narcotics (eg, fentanyl and remifentanil).
      4. Increased vagal tone occurs with traction on the peritoneum or spermatic cord; pressure on the globe via the oculocardiac reflex; pressure near the brainstem during craniotomies for posterior fossa lesions; direct pressure on the vagus nerve or carotid sinus during neck or intrathoracic surgery; acute distension of the peritoneal cavity during laparoscopy; centrally mediated vagal response from anxiety or pain (vasovagal reaction); and Valsalva maneuvers.
      5. Increased intracranial pressure (Cushing reflex).
      6. Reflex bradycardia. From baroreceptor reflex (eg, with phenylephrine administration), atrial stretch, or cardiopulmonary reflex.
    2. Treatment of sinus bradycardia
      1. Verify adequate oxygenation and ventilation.
      2. Bradycardia due to increased vagal tone requires discontinuation of the provocative stimulus. The vagal reflex may fatigue with repeat stimulus or be less pronounced with deeper anesthesia. Atropine 0.5 mg IV or low-dose epinephrine 10 to 50 μg IV may be needed if the patient is hypotensive. Glycopyrrolate 0.2 to 0.6 mg IV or ephedrine 5 to 10 mg IV may be given for hemodynamically stable bradycardia.
      3. In patients with intrinsic cardiac disease, treatment should proceed with atropine 0.5 mg IV, chronotropes (eg, ephedrine, dopamine), or cardiac pacing.
  2. Sinus tachycardia is a sinus node–driven heart rate greater than 100 beats/min. The rate is regular and rarely exceeds 160 beats/min. Electrocardiogram (ECG) should demonstrate a P wave preceding each QRS complex with a fixed PR interval.
    1. Etiologies: Catecholamine excess, inadequate anesthesia or analgesia, hypercarbia, hypoxia, hypotension, hypovolemia, medications (eg, pancuronium, desflurane, atropine, and ephedrine), fever, MI, PE, tamponade, tension pneumothorax, malignant hyperthermia, pheochromocytoma, and thyrotoxicosis.
    2. Treatment should be directed toward correcting the underlying cause and may include the following:
      1. Correcting oxygenation and ventilation abnormalities.
      2. Increasing the depth of anesthesia and treating pain with analgesics.
      3. Correcting hypovolemia.
      4. Medications such as opioids and β-adrenergic blockers. Patients with active coronary artery disease and adequate blood pressure may benefit by treatment with β-adrenergic blockers to control the heart rate while the cause is being determined.
  3. Heart block
    1. First-degree atrioventricular (AV) block is characterized by a PR interval of 0.2 seconds or longer. In first-degree block, every atrial pulse is transmitted to the ventricle.
    2. Second-degree AV block is divided into two types: Mobitz type 1 (Wenckebach) and Mobitz type 2.
      1. Mobitz type 1 (Wenckebach) usually occurs when a conduction defect is in the AV node and is manifested by a progressive PR prolongation culminating in a nonconducted P wave. It is generally benign.
      2. Mobitz type 2 is a conduction defect often distal to the AV node. It presents with a constant PR interval and frequent nonconducted P waves. It is more likely to progress to third-degree block.
    3. Third-degree AV block (complete heart block) may be caused by intrinsic AV nodal or His Purkinje disease and occurs when there is complete failure of any conduction from the atria to ventricles. It presents with AV dissociation (variable PR intervals) and either a junctional (narrow QRS) or ventricular (wide QRS) escape rhythm. For a quick reference, please see uptodate.com’s ECG tutorial on atrioventricular block.
    4. Treatment of heart block
      1. First-degree AV block does not usually require specific treatment; however, temporary pacing should be available in the case of first-degree heart block in combination with a bifascicular block (so-called trifascicular block).
      2. Second-degree AV block
        1. Mobitz type 1 requires treatment only if the patient becomes symptomatic or hemodynamically unstable. Temporary transcutaneous or transvenous pacing may be necessary, particularly during an inferior MI, although the block may resolve following revascularization
        2. Mobitz type 2 may progress to complete heart block. Hemodynamically unstable patients should be urgently treated with atropine and often temporary cardiac pacing. Stable patients should be continuously monitored for progress to higher-grade conduction block warranting evaluation for pacemaker placement while being evaluated for stable causes.
      3. Third-degree AV block is treated with transcutaneous, transvenous, or epicardial pacing.
  4. Supraventricular tachycardias (SVTs) originate at or above the bundle of His. The resulting QRS complexes are narrow (<120 ms) except during aberrant conduction.
    1. Atrial premature contractions (APCs or PACs) occur when ectopic foci in the atria fire before the next expected impulse from the sinus node. The P wave of an APC characteristically looks different from preceding P waves, and the PR interval may vary from normal. APCs may cause aberrant QRS complexes. If the AV node is still in a refractory period, an APC will not elicit a ventricular response. APCs are common, usually benign, and typically require no treatment.
    2. Junctional or AV nodal rhythms are characterized by absent or abnormal P waves and normal QRS complexes. Although they may indicate ischemic cardiac disease, junctional rhythms are commonly seen in healthy individuals receiving inhalational anesthesia. In the patient whose cardiac output depends heavily on the contribution from atrial contraction, stroke volume and blood pressure may decline precipitously. Treatment may include the following:
      1. Reduction of anesthetic depth.
      2. Increasing intravascular volume.
      3. Atropine in increments of 0.2 mg IV may convert a slow junctional rhythm to sinus rhythm, particularly if secondary to a vagal mechanism.
      4. Paradoxically, β-blockers may be used cautiously (eg, propranolol 0.5 mg IV and metoprolol 1-3 mg), especially with isorhythmic AV dissociation (independent atrial and ventricular rhythms that are similar in rate).
      5. If the dysrhythmia is associated with hypotension, increasing the blood pressure with vasopressors (eg, ephedrine or norepinephrine) may be required as a temporizing measure.
      6. If necessary, atrial pacing may be instituted to restore atrial contraction.
    3. Atrial fibrillation is an irregular rhythm with an atrial rate of 350 to 600 beats/min and a variable ventricular response. It may be seen with myocardial ischemia, mitral valvular disease, hyperthyroidism, PE, excessive sympathetic stimulation, and digitalis toxicity; after thoracic surgery; or when the heart has been manipulated. Treatment is based on the hemodynamic status.
      1. Rapid ventricular rate with stable hemodynamics can be treated initially with β-adrenergic blockade, such as propranolol 0.5-mg increments IV, metoprolol 2.5- to 5-mg increments, esmolol 5- to 10-mg increments, or a calcium channel blocker such as verapamil 2.5- to 5-mg increments or diltiazem 10 to 20 mg IV (see Chapters 18 and 39). Amiodarone 150 mg IV can be used to promote conversion back to sinus rhythm (anticoagulation prior to cardioversion is recommended in patients with atrial fibrillation for longer than 24 hours).
      2. Rapid ventricular rate with unstable hemodynamics requires synchronized cardioversion (50-100 J if biphasic or 200 J if monophasic) (see Chapters 18 and 39).
    4. Atrial flutter is usually a regular rhythm with an atrial rate of 250 to 350 beats/min and a characteristic sawtooth ECG configuration. It is often seen with underlying heart disease (ie, rheumatic heart disease and mitral stenosis). Conduction across the AV node is often 2:1 in patients not taking AV nodal blockers, but it may also be 1:1 or 4:1. A 2:1 block will result in a rapid ventricular rate (usually 150 beats/min). Treatment usually includes β-adrenergic, calcium channel blockade, or synchronized cardioversion (see Chapters 18 and 39).
    5. Paroxysmal SVT is an abrupt-onset tachydysrhythmia (atrial and ventricular rates of 150-250 beats/min) with reentry usually through the AV node. This rhythm may be associated with Wolff-Parkinson-White (WPW) syndrome, thyrotoxicosis, or mitral valve prolapse. Patients without heart disease may develop this dysrhythmia owing to stress, caffeine, or excess catecholamines.
      1. Hemodynamically unstable patients with SVT should undergo synchronized cardioversion starting at 50 to 100 J. These patients are at high risk for ventricular fibrillation.
      2. For hemodynamically stable patients with SVT, treatment includes adenosine 6 to 18 mg IV, Valsalva maneuvers, carotid sinus massage, or propranolol 1 to 2 mg IV.
      3. For patients with WPW syndrome, AV nodal blockers (including adenosine, calcium channel, and β-blockers) are contraindicated for the treatment of atrial fibrillation or atrial flutter as they selectively slow conduction through the AV node, which can lead to increased conduction through the accessory pathway and cause ventricular fibrillation.

        Options for rhythm control in hemodynamically stable patients with WPW include procainamide 20 to 50 mg/min (until arrhythmia terminates, hypotension ensues, QRS is prolonged by >50%, or total of 17 mg/kg dose is reached) or ibutilide (for patients <60 kg, 0.01 mg/kg infused over 10 minutes; for patients >60 kg, 1 mg over 10 minutes). If the arrhythmia does not terminate within 10 minutes after the end of the infusion, a second bolus may be given).

  5. Ventricular dysrhythmias
    1. Ventricular premature contractions (VPCs or PVCs) occur when ectopic foci in the ventricle fire before the next expected impulse arrives. They are characterized by widened QRS (>120 ms) complexes. When these are coupled alternately with normal beats, ventricular bigeminy exists. VPCs are occasionally seen in healthy individuals but carry a worse prognosis in patients with underlying heart disease. Under anesthesia, they frequently occur during states of catecholamine excess, hypoxia, or hypercarbia. They may also signify myocardial ischemia or infarction, heart failure, digitalis toxicity, hypokalemia, or hypomagnesemia. VPCs may require therapy when a patient becomes hemodynamically unstable. Other concerning features include sustained durations, increase in frequency (>10% of all ventricular depolarizations), or occurrence on or near the preceding T wave (R-on-T phenomenon); these situations may precede the development of ventricular tachycardia, ventricular fibrillation, and cardiac arrest.

      Treatment in an otherwise hemodynamically stable patient should begin with ensuring adequate depth of anesthesia, oxygenation, and ventilation and assessing for electrolyte abnormalities (especially potassium and magnesium). Patients with coronary artery disease who continue to have ventricular irritability should have any ischemia treated. If the ectopy continues, then amiodarone (150 mg IV over 10 minutes followed by an infusion at 1 mg/min for 6 hours then 0.5 mg/min thereafter) may be considered. Refractory ventricular ectopy may require further treatment (see Chapters 18 and 39).

    2. Ventricular tachycardia is defined as three or more successive ventricular complexes. Nonsustained VT is three or more repetitive ventricular beats with a duration of <30 seconds. Sustained VT lasts for >30 seconds or is associated with hemodynamic impairment. Monomorphic VT is the repetition of the same basic QRS complex, whereas polymorphic VT refers to changing QRS morphology particularly if there is a change in axis. Polymorphic VT with a prolonged baseline QTc is called torsades de pointes.
      1. Hemodynamically unstable patients with a pulse should be treated as outlined in the advanced cardiac life support (ACLS) guidelines with cardiopulmonary resuscitation and cardioversion (120-200 J if biphasic, or 360 J if monophasic; if unresponsive, may increase energy in a stepwise fashion).
      2. For stable patients with sustained monomorphic VT, pharmacologic cardioversion can be attempted, but the patient should be monitored carefully as patients who are hemodynamically stable initially can rapidly become unstable. Underlying causes such as electrolyte disturbance, ischemia, and heart failure should also be treated.
      3. Polymorphic VT is usually a hemodynamically unstable rhythm requiring urgent defibrillation.
      4. In conscious, stable patients with torsades de points, intravenous magnesium sulfate is often an effective therapy.
    3. Ventricular fibrillation is chaotic ventricular activity resulting in ineffective ventricular contractions. Prompt defibrillation is required with the same starting energy as above.
    4. Pre-excited atrial fibrillation. In patients with a wide-complex tachycardia who are hemodynamically stable, consider pre-excited atrial fibrillation. Initial therapy with rhythm or rate control should be attempted (refer to WPW syndrome above).