Lecture of bradycardia

2021-01-28 12:00 AM

A 12-lead electrocardiogram is important in classifying bradycardia and helps diagnose causes such as myocardial infarction, myocarditis.


Normal heart rate ranges from 60 to 80 times/minute. Considered bradycardia when the heart rate decreases <50 beats/min. Bradycardia often leads to a lack of blood supply to the brain leading to dizziness, confusion, fainting, if severe, cerebral vascular accidents.

 Bradycardia vs Normal heart beat

Anatomy of the heart's pacing and conduction systems

Under normal circumstances, the heart is controlled by impulses emanating from the sinus node located below the extracellular layer, the connection between the superior vena cava and the right atrium. The impulse is then propagated through the atria to the atrioventricular node, across the bundle of His to the right and left branches so that the Purkinje network ends up forming synchronous depolarization and, in the atria, and ventricles, respectively, expressed on the electrocardiogram. The graph is the P, QRS, and T waves.

In some pathological conditions, impulses may also originate from the atria, atrioventricular node, or from ventricles.

In addition to the normal pathways, in some people, there are also auxiliary pathways such as Kent, Mahaim, Brechenmacher, ...

The formation and conduction of impulses in the heart are also governed by the sympathetic and parasympathetic nervous systems.

Pathogenesis of bradycardia

The mechanism of disturbance in impulse formation such as sinus arrest, sinus node failure.

Mechanism of impulse conduction disorders such as sinus block, atrioventricular block.

Neurological and humoral mechanisms such as increased sensitivity of the carotid sinuses, caused by X nerve


A bacterial or viral infection.

Myocardial anemia or myocardial infarction.

Autoimmune pathology.

Degenerative connective tissue pathology.

After heart surgery or electrophysiological resection.


Due to drugs: Digoxin poisoning, inhibitors? calcium inhibitors, antiarrhythmic drugs.

Due to electrolyte disturbances such as hyperkalemia/blood.

But sometimes the cause is also unknown.

Part slow beat

Sinus bradycardia.

Sinus arrest.

Atrial sinus block I.

Atrial sinus block II.

Atrial sinus block III.

Grade I atrioventricular block.

Grade II atrioventricular block.

High-grade atrioventricular block.

Grade III atrioventricular block.

Alternating branch block.

Atrial fibrillation with a slow ventricular response.


Medical history

Often vague and poor, with symptoms of cerebral ischemia such as dizziness, dizziness, fainting, convulsions, heart symptoms such as fatigue, shortness of breath, chest tightness, feeling of heart beating slow, irregular.

Clinical examination

Often also poor symptoms of slow, steady or irregular heartbeats, symptoms of heart failure if bradycardia persists.

Special attention should be paid to look for cannonballs (bruit de canon), or carotid vein retrograde signs, suggesting separation between the atria and ventricles.


12-lead ECG: very important in classifying bradycardia and helping diagnose causes such as myocardial infarction, myocarditis ... In many cases, it is also necessary to measure a prolonged lead or measure a more special lead to clear the rules.

24-hour ECG: very useful if routine ECG does not give a clear result.

Exercise ECG: has also been useful in detecting bradycardia or arrhythmias occurring during exercise, and poor heart rate response during exercise.

Electrophysiological investigation of the heart to evaluate the function of the formation and conduction of impulses.

The tilt test is intended to determine the causes of neurologic humor.

Echocardiography: often plays a less important role in bradycardia.


Drug treatment

Atropine: drug has competitive inhibitory effect with Acetylcholine at M2 receptors of the myocardium, causing inhibition of parasympathetic activity, dose: 0.5mg q5-10 minutes total dose 2mg (0.04 mg/kg), contraindications: closed-angle glaucoma, prostate fibroids.

Isoproterenol: non-selective sympathomimetic stimulant effect, a dose of 0.5-5µg / min TTM, contraindicated: acute myocardial infarction, progressive angina.

Epinephrine: has a stimulant effect? sympathomimetics, dose 2-10µg / min TTM

Dopamine: has a stimulant effect? communion and both? sympathomimetics at high doses, dose of 5-20µg / kg / min TTM

Xanthine oxidase group such as Theophylline and sympathomimetic β 2 stimulant group such as salbutamol used by mouth in cases of sinus bradycardia or mild sinus node failure.

Put on the pacemaker

Set up a temporary pacemaker:

Intravenous or over pericardial electrodes, or stimulation via chest patches, is indicated when bradycardia is temporary in cases of myocarditis, acute myocardial infarction, poisoning. drugs, electrolyte disturbances, post-surgery, ..., or in an emergency situation put temporary and permanent placement.

Set the permanent pacemaker:


Symptomatic sinus bradycardia or atrial block.

Sinus bradycardia when using drugs that must be used.

Symptomatic frequency response is poor.

Accompanying atrioventricular block.

Unconsciousness> 3 seconds while awake.

Exit rate <40 times / minute.

Atrioventricular node ablation.

Neuromuscular disease.

Atrioventricular block after heart surgery does not hope to recover.

Atrial bloc or atrium-atrial intermittent (Grade II Mobitz II or Grade III)

Bloc alternating branches.

Fainting when rubbing the carotid sinus with systolic> 3 seconds.