Sinus bradycardia: definitions, ECG, causes and management

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Sinus bradycardia: ECG, causes & management

Definition of sinus bradycardia

Sinus bradycardia fulfills the criteria for sinus rhythm but the heart rate is slower than 50 beats per minute. ECG criteria follows:

Regular rhythm with ventricular rate slower than 50 beats per minute.
P-waves with constant morphology preceding every QRS complex.
P-wave is positiv in limb lead II.

Normal (physiological) causes of sinus bradycardia

Sinus bradycardia (SB) is considered a normal finding in the following circumstances:

During sleep.
Well-trained individuals display SB at rest due to high vagal tone. These individuals have developed a highly efficient left ventricle, capable of generating sufficient cardiac output at low heart rates.
During vasovagal syncope (e.g during intense emotional stress)
During vagal maneuvers (Valsalva maneuver, carotid sinus [baroreceptor] stimulation).
Its not uncommon to discover SB in healthy young individuals who are not well-trained. This is also a normal finding.

Abnormal (pathological) causes of sinus bradycardia

In all other situations, sinus bradycardia should be regarded as a pathological finding. There are numerous pathological conditions that cause sinus bradycardia. The most important causes are as follows:

Myocardial ischemia/infarction – Particularly ischemia or infarction located to the inferior wall of the left ventricle. This type of bradycardia is due to diminished automaticity (pacemaker function) in the sinoatrial node or conduction defects (e.g second-degree AV block) as a result of ischemia/infarction.
Sinus Node Dysfunction (SND) – Sinus node dysfunction implies that the cells of the sinoatrial node are defect and fail to generate electrical impulses.
Side effects of drugs (notably beta blockers, digitalis, verapamil, diltiazem, amiodarone, klonidin) – These drugs affect the pacemaker cells in the sinoatrial node. They may also induce conduction defects (e.g AV block).
Increased intracranial pressure (manifests with sinus bradycardia and hypertension).
Hypothyroidism.
Hypothermia.
Hyperkalemia.

ECG example of sinus bradycardia

Figure 1 shows sinus bradycardia at paper speed 25 mm/s.

Figure 1. Sinus bradycardia. Paper speed 25 mm/s. Calculate the rate by dividing 300 by the number of large boxes between two cycles (e.g between two R waves). As seen in the figure, there are approximately 6.5 large boxes between two R waves. 300/6.5 equals 46 beats/min. Click to zoom.

Figure 2. Sinus bradycardia, premature ventricular contractions, incomplete right bundle branch block and ST-segment depressions in V2-V6. — Figure 2. Sinus bradycardia, two premature ventricular contractions, incomplete right bundle branch block and ST-segment depressions in V2-V6. Click to zoom.

Figure 3. Sinus bradycardia. The small q-waves in inferior leads (II, aVF, III) are not significant. Low voltage in limb leads. Click to zoom.

Figure 4. Sinus bradycardia. Click to zoom.

Treatment of sinus bradycardia: general aspects of management

Benign causes of sinus bradycardia (SB) do not require treatment. In all other situations it is necessary to find the underlying cause and direct treatments towards it. The most common causes are sinus node dysfunction, side effects of medications or acute myocardial ischemia/infarction. When the bradycardia causes hemodynamic symptoms it should be treated. Note that sinus bradycardia due to ischemia located to the inferior wall of the left ventricle is typically temporary and resolves within 1–2 weeks (sinus bradycardia due to infarction/ischemia is discussed separately).

Benign (physiological) causes of bradycardia (e.g vasovagal reaction, well-trained athletes) need not be treated. When in doubt whether the bradycardia is physiological, it is useful to perform a Holter ECG (ambulatory recording). If drug side effects are believed to be the cause, it is fundamental to judge the risk of terminating drug therapy as compared with implementing an artificial pacemaker in order to be able to continue drug therapy. It is very common that patients with bradycardia have a strong indication for drugs that aggravate or even cause the bradycardia; in such scenarios, it is generally considered to be evidence based to implement an artificial pacemaker that will allow for drug therapy to continue.

Sick sinus syndrome (sinus node dysfunction), which is a common cause of bradycardia, is also discussed separately.

Algorithm for acute management of bradycardia

Terminate or adjust any medications that cause or aggravate the bradycardia.
In case of acute bradycardia with circulatory compromise:
- (1) 1–2 ml of atropine 0.5 mg/ml is the first line therapy. It can be repeated if necessary.
- (2) If atropine is insufficient or require too frequent dosing, infusion isoproterenol should be given. An ampoule with 5 ml (0,2 mg/ml) isoproterenol is mixed with 245 ml glucose (50 mg/ml) with starting dose 0,01 μg/kg/min. This is titrated up until adequate effect is achieved.
- (3) If atropine and isoproterenol fails, it might be necessary to perform transcutaneous pacing (external pacing). Most modern defibrillators are equipped with ability to perform transcutaneous pacing. Transcutaneous pacing is only indicated until a permanent pacemaker can be implemented.
- (4) An alternative to transcutaneous pacing is temporary transvenous pacing, which is also indicated until a permanent pacemaker can be implemented.

Patients with bradycardia due to myocardial ischemia/infarction only demand treatment if cardiac output is compromised or if the bradycardia predisposes to more malign arrhythmias (the algorithm above applies to this situation as well). Note, however, that bradycardias due to inferior wall ischemia/infarction is transient in most cases and rarely necessitate permanent pacemaker. Anterior wall infarctions, on the other hand, generally leave permanent bradycardia and thus demand permanent pacemaker. Learn more about conduction defects caused by ischemia and infarction.

Permanent (long-term) treatment of bradycardia

Permanent symptomatic bradycardias are treated with artificial pacemakers. Note that patients with chronotropic incompetence may require pacemaker to increase exercise capacity and reduce symptoms. Patients with tachy-brady syndrome may also necessitate rate controlling drugs (e.g beta-blockers) and anticoagulation (if atrial fibrillation or flutter can be verified).