Bradycardia



Bradycardia


Andrea Corrado

Gianni Gasparini

Antonio Raviele



SINUS RHYTHM

The electrical activation of the heart originates spontaneously from the cells of the sinoatrial node (SAN), which is situated at the junction between the right atrium and the superior vena cava and has a frequency between 60 and 100 bpm. For this reason, the normal rhythm of the heart is called sinus rhythm. If the frequency of the sinus rhythm is lower than 60 or higher than 100 bpm, the term sinus bradycardia or sinus tachycardia is used (Fig. 1-1).


SINUS BRADYCARDIA

Sinus bradycardia is often a physiological phenomenon, particularly in vagotonic subjects (e.g., athletes). Sometimes, it is secondary to the action of pharmaceutical drugs (digitalis, β-blockers, or calcium antagonists). In some subjects, it may be a manifestation of SAN dysfunction. In the latter case, the bradycardia is more marked (<50 bpm) and is associated with other electrocardiographic expressions of SAN disease, such as sinoatrial block and/or atrial tachyarrhythmia (atrial fibrillation or flutter).


AUTONOMIC BLOCKADE

To distinguish sinus bradycardia due to SAN dysfunction from sinus bradycardia due to vagal hypertonia, it may be useful to elicit a so-called autonomic blockade, which involves evaluating the heart rate during the simultaneous administration of a β-blocker (propranolol 0.2 mg/kg) and atropine (0.04 mg/kg). The objective is to “block” the influence of the autonomic system (sympathetic and parasympathetic) on the heart rate, thereby uncovering the “intrinsic” SAN frequency. The following formula enables us to calculate the heart rate (X) that can be regarded as normal during autonomic blockade:

118.1 – (0.57 × age) = X ± 14% (normal heart rate)

A heart rate below this value in patients aged less than 45 years (or ±18% in patients >45 years) is indicative of SAN dysfunction.







Figure 1-1 From the SAN, the impulse travels along preferential pathways made up of specialized fibrous cells to the atria (A), AVN, His bundle and its branches, and finally to the ventricular myocardium (V). This sequence of electrical activation occurs in little more than 200 ms; on the surface ECG, it generates the P wave, the PR interval, and the QRS complex in succession.


SINOATRIAL BLOCK

Sinoatrial block is defined as the lack of transmission to the atria of the impulses generated by the SAN. There are various degrees of sinoatrial block.

First-degree sinoatrial block: Delayed propagation of the impulse from the SAN to the atria (this condition is not recognizable on surface ECG).

Second-degree Wenckebach sinoatrial block: (Fig. 1-2). In the presence of a “typical” Wenckebach sinoatrial block, three characteristic phenomena can be observed:



  • the PP intervals are progressively reduced before the pause,


  • the pause is less than twice the interval that precedes it, and


  • the PP interval following the pause is longer than the PP interval that precedes it.

Second-degree Mobitz sinoatrial block: (Fig. 1-3). Unlike second-degree Wenckebach sinoatrial block, in this case,



  • the PP intervals are not progressively reduced since the pause,


  • the pause is equal to twice the interval that precedes it, and


  • the PP interval following the pause is not longer than the PP interval that precedes it.

2:1 sinoatrial block: (Fig. 1-4).

Third-degree sinoatrial block: (Fig. 1-5).

Sinus arrest: The lack of formation of the sinus impulse is a very rare condition. Indeed, it is very unlikely that none of the cells that make up the SAN will be able to generate an electrical impulse. Electrocardiographically, this form is indistinguishable from third-degree sinoatrial block.







Figure 1-2 Second-degree Wenckebach sinoatrial block. Propagation of the impulse from the SAN to the atria progressively slows down and is finally interrupted.






Figure 1-3 Second-degree Mobitz sinoatrial block. Sudden lack of conduction of a sinus impulse without progressive lengthening of conduction time.






Figure 1-4 2:1 sinoatrial block is characterized by the lack of conduction to the atria of each alternate impulse (on surface ECG, bradycardia is indistinguishable from sinus bradycardia owing to reduced SAN automaticity).







Figure 1-5 Third-degree sinoatrial block. In this condition, no sinus impulse is conducted to the atria. In such cases, a junctional escape rhythm generally emerges.


SINUS NODE—CORRECTED RECOVERY TIME AND SINOATRIAL CONDUCTION TIME

In patients with clinical and electrocardiographic signs of suspected SAN dysfunction, it may be useful to perform an endocavitary electrophysiological study to calculate the corrected sinus node recovery time (CSNRT) and the sinoatrial conduction time (SACT).

CSNRT: (Fig. 1-6 A). The postpacing pause represents the sinus node recovery time (SNRT). This interval is then “corrected” on the basis of the spontaneous rhythm according to the following formula:

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Oct 27, 2018 | Posted by in CARDIOLOGY | Comments Off on Bradycardia

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