Bradycardic Rhythms

Info

🌱 來自: Huppert’s Notes

Bradycardic Rhythms🚧 施工中

Bradycardic Rhythms

Sinus bradycardia

•   ECG: See Figure 1.14

FIGURE 1.14: ECG examples of common bradyarrhythmias and tachyarrhythmias.

•   Physiologic causes: (Vast majority) Increased vagal tone or decreased sympathetic tone:

-   Sleep (HR can fall to 35–40 bpm normally, especially in young patients and those with OSA)

-   Well-conditioned athletes

-   Vasovagal episodes (e.g., vomiting, Valsalva)

-   Cushing’s reflex due to increased intracranial pressure

-   Reflex bradycardia from severe hypertension

•   Pathologic or extrinsic causes:

-   Medications (e.g., beta blockers, calcium channel blockers, clonidine, digoxin, amiodarone, timolol eye drops)

-   Ischemia (especially inferior MI)

-   Infiltrative diseases (e.g., sarcoid, amyloid)

-   Hypothermia, hypothyroidism, hypokalemia, hypoxia (if severe, prolonged)

•   Treatment:

-   Asymptomatic or transient: No treatment required (majority of cases)

-   Symptomatic: Dizziness, hypotension, altered mental status

•   If unstable, give atropine and consider pacing as discussed above. Treat underlying problem. If beta blocker overdose, give glucagon. If calcium channel blocker overdose, give CaCl2. Rarely, consider pacemaker placement.

Sinus arrhythmia

•   Definition: Phasic variation in the sinus cycle; respiratory (variation with breathing) or nonrespiratory (variation not associated with breathing)

•   Epidemiology: Most frequent arrhythmia; normal and common in young patients or those with high vagal tone

Sick sinus syndrome

•   Definition: Nonspecific term referring to any or multiple of the following:

-   Persistent pathologic/symptomatic sinus bradycardia

-   Sinus arrest

-   SA exit block

-   Combinations of sinus and AV conduction disorders

-   Tachy-brady syndrome: Patients who alternate between any bradycardic rhythm and tachycardic rhythm (e.g., alternating paroxysmal Afib with RVR and symptomatic sinus bradycardia)

•   Treatment: Consider pacemaker placement if symptomatic or associated with high-degree AV block

AV blocks

•   First degree: Delayed conduction at the AV node. Prolonged PR (>200 ms), all atrial impulses conducted (1:1). Patients are usually asymptomatic and no treatment is necessary. Caution with use of beta blockers, calcium channel blockers.

•   Second degree: Intermittent failure of conduction between the atria and ventricles (Figure 1.14).

-   Mobitz Type I (Wenckebach): Lengthening of PR until impulse not conducted and “dropped” beat (compare first/last). Usually a nodal block due to problems with the AV node itself (e.g., AV node damage due to ischemia/inflammation) or due to increased vagal tone (e.g., with sleep, drugs). Improves with atropine/exercise, worsens with carotid massage. No treatment needed unless symptomatic. Consider atropine and stop AV nodal blockers.

-   Mobitz Type II: No change in PR length but then sudden dropped beat. Usually an infranodal block, meaning that the issue is in the His-Purkinje system beneath the AV node (e.g., due to age, ischemia, aortic valve surgery). Improves with carotid massage, worsens with atropine/exercise. Can progress to third-degree block. Treatment: Pacemaker (Table 1.7).

TABLE 1.7 • Pacemakers: Indications and Types

•   Third degree (complete): No AV conduction; no relationship between P and QRS (Figure 1.14). Escape, if present, is narrow (junctional) or wide (ventricular). Differential diagnosis: Ischemia, aging, lyme disease. Treatment: Pacemaker (Table 1.7).