Bradyarrhythmias




























Sick sinus syndrome
Infiltrative diseases (e.g., sarcoidosis)
Collagen vascular diseases (e.g., scleroderma)
Atrioventricular conduction block
Acute or chronic ischemic heart disease
Increased vagal tone (e.g., Valsalva maneuver)
Drugs (e.g., digoxin, beta-blockers)
Obstructive sleep apnea
Hypothyroidism
Hypothermia
Vector-borne illness (e.g., Lyme disease)
Increased intracranial pressure (i.e., Cushing reflex)
Electrolyte disturbances (e.g., hypo/hyperkalemia)



Presentation


Classic presentation


  • Although the symptoms are nonspecific, many will be related to inadequate cardiac output secondary to the low heart rate:

    • Orthostatic hypotension
    • Dizziness
    • Syncope
    • Generalized fatigue or malaise
    • Chest pain
    • Shortness of breath

Critical presentation


  • Sinus bradycardia occurs in 15–20% of patients with acute myocardial infarction secondary to ischemia of the SA node.
  • Syncope may result from primary dysrhythmia or from reduced cardiac output.
  • Hemodynamic instability:

    • Similarly to patients with rapid heart rates, instability is defined as the evidence of hemodynamic compromise with a discernible pulse.
    • Patients will present with hypotension, altered mental status, ischemic chest pain, or respiratory distress from congestive heart failure and pulmonary edema.
    • Patients who do not have a palpable pulse are in cardiac arrest and are treated according to ACLS guidelines.

Diagnosis and evaluation



  • A 12-lead electrocardiogram (ECG) is essential for the diagnosis of bradycardia and to differentiate between the different types of bradyarrhythmias.
  • History should focus particularly on symptoms of ischemic heart disease, and on medications such as nodal blockers.
  • Some laboratory values may be helpful, depending on the suspected etiology:

    • Troponin to assess for myocardial injury
    • Electrolytes to rule out hyperkalemia from changes in renal function
    • Digoxin level if appropriate
    • Thyroid-stimulating hormone (TSH).

  • A rectal temperature should be taken to rule out hypothermia as a possible etiology.
  • Once the ECG is performed, further information about the location and severity of the conduction delay can be obtained.

    • SA node dysfunction:

      • Irregular or absent sinus node activity.
      • Most common reason for pacemakers in the United States.
      • “Sick sinus syndrome”:

        • Caused by a worsening fibrosis of the SA node or diminished blood flow to the SA nodal artery.
        • Most often seen in patients older than 70 years old.
        • Characteristics include inappropriate bradycardia, alternating bradycardia and tachyarrhythmias, and/or sinus pauses or sinus arrest.

  • AV node dysfunction:

    • AV conduction blocks can be either transient or permanent and can result from numerous etiologies.
    • The most common cause of AV nodal dysfunction is ischemic disease (40%), though other etiologies are possible:

      • Idiopathic fibrosis of the conduction system
      • Bacterial endocarditis
      • Vector-borne disease
      • Medication overdose

  • AV node dysfunction can be classified as first-degree, second-degree (types I and II) or third-degree (i.e., complete heart block).

    • First-degree AV block:

      • Defined as a PR interval of greater than 200 milliseconds.
      • Each P is associated with a QRS and both the P-P and R-R intervals remain constant.
      • It is generally considered to be benign.

  • Second-degree AV block: Mobitz type I (aka: Wenckebach (see Figure 22.1):

    • Defined as a rhythm with an increasingly prolonged PR interval that will eventually lead to a dropped beat.
    • This pattern can happen intermittently or persistently, and in a variety of groupings.
    • Like first-degree AV blocks it is generally considered to be benign and does not require intervention.

  • Second-degree AV block: Mobitz type II (see Figure 22.2):

    • Defined as a consistent PR interval with intermittent failure of conduction through the AV node resulting in dropped beats.
    • Can be seen in grouped beats as type I, but can also have varying degrees of block.
    • Frequently progresses to complete heart block (third-degree heart block).
    • Due to the potential for progression of the blockade, these patients require admission to the hospital and evaluation for a pacemaker.

  • Third-degree AV block (complete heart block) (see Figure 22.3):

    • Defined as a complete disassociation between atrial and ventricular activity.
    • No relationship exists between P-waves and the QRS complexes.
    • Ventricular escape beats can originate anywhere from the AV node (narrow complex) to the Purkinje system (wide QRS complex).
    • A permanent pacemaker is indicated in the setting of this rhythm.


Figure 22.1. Second-degree AV block: Mobitz type I (Wenckebach).

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Feb 17, 2017 | Posted by in CRITICAL CARE | Comments Off on Bradyarrhythmias

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