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Sinus Bradycardia

normal
Lead II
25 mm/s10 mm/mV
HR72bpm
RR833ms
QT368ms

Normal sinus rhythm under 60 bpm: the same beat, the same intervals, only further apart.

Updated

On the trace

Read the strip in this order.

Try each step, then check it.
  1. Take the rate.
    Show 50 bpm, R-R 1200 ms. Under 60 is the whole diagnosis, and everything else on this strip is there to confirm that nothing else is wrong.
  2. Find the P waves.
    Show One before every QRS, upright, 0.18 mV, identical in shape. The sinus node is still in charge. It is simply firing more slowly.
  3. Measure the PR.
    Show 175 ms, fixed. Slow because the node is slow, not because conduction is delayed. A bradycardia with a lengthening PR is a block, not this.
  4. Measure the QRS.
    Show 74 ms, narrow. Nothing about the conduction system has changed.
  5. Compare it with a normal strip.
    Show The complexes are the same shape and the same width, only further apart. That is what makes this benign in a way that a slow rhythm from a lower pacemaker is not.
The full pictureNormal Sinus RhythmThe P wave, PR interval and QRS are unchanged from normal sinus rhythm, which is where those are described.

How to recognise it

FeatureValueNotes
RateUnder 60 bpm50 here. Below about 40, look hard for a non-sinus escape rhythm instead.
P waveUpright, one per QRSUnchanged from sinus. Its presence is what makes this sinus bradycardia.
PR interval120 to 200 ms, fixed175 here. A PR that moves is a block.
QRSNarrow, 74 ms hereWide raises the question of an escape rhythm rather than a slow sinus one.
RhythmRegularIrregularity at a slow rate suggests pauses or block.
T waveTaller at slow rates0.28 mV here against 0.18 at 72. A longer diastole, not a change in repolarisation.

The strip

Thirty seconds of sinus bradycardia in lead II, drawn by the simulator. Work through the steps above on it: take the rate, then confirm the P, PR and QRS are otherwise normal.

Mechanism

The sinus node fires whenever its cells drift up to threshold, and how fast they drift is set almost entirely by the autonomic nervous system. Vagal traffic slows the drift, sympathetic traffic speeds it. Anything that raises vagal tone or blocks sympathetic drive therefore slows the rate without changing anything about how the impulse travels afterwards.

That is why the beat looks identical. The node is the only part of the system behaving differently, so only the spacing changes.

Go deeper

When a slow rate is a fit heart

Endurance training raises resting vagal tone and enlarges stroke volume, so a trained athlete maintains cardiac output at 40 to 50 beats a minute and is entirely well. Sleep does the same thing temporarily in everyone. A rate that would be alarming in a breathless patient is unremarkable in a resting runner, which is why the number never decides this on its own.

The drugs, and the one that is not a drug

Beta-blockers, non-dihydropyridine calcium-channel blockers, digoxin, amiodarone, ivabradine and clonidine all slow the node. So do hypothyroidism, hypothermia, raised intracranial pressure and obstructive sleep apnoea. In an older patient with none of these, the question becomes whether the node itself is failing.

Sick sinus syndrome

A node that has become unreliable produces bradycardia that does not respond to demand, often alternating with atrial tachyarrhythmias, which is the tachycardia-bradycardia syndrome. The giveaway is a rate that does not rise with exertion, so exercise testing is often more informative than a resting ECG.

The inferior infarct

The right coronary artery supplies the sinus node in most people, so bradycardia within hours of an inferior infarct is common, usually vagally mediated, and usually transient. It often responds to atropine and rarely needs pacing, which is the opposite of the bradycardia that accompanies an anterior infarct.

Clinical impact

Vagal tone, a drug or nodal disease slows the sinus node
Conduction below the node is untouched, so the beat is unchanged
A trained or sleeping heart maintains output easilyOften normal
When stroke volume cannot compensate, output falls with the rateWatch

The rhythm matters only when the patient does. Dizziness, breathlessness, confusion, chest pain or hypotension turn a number into a diagnosis.

Management

1

Ask whether the patient has symptoms

An asymptomatic rate of 50 in a well person needs nothing at all. This is the first question and it settles most cases.

2

Review the drug list before anything else

Rate-slowing drugs are the commonest reversible cause, and stopping or reducing one is usually enough.

3

Atropine, then pacing, if the patient is compromised

Standard bradycardia management. Atropine works here because the block is at the node, where vagal tone acts.

4

Investigate a node that will not speed up

A rate that fails to rise with exertion points at sinus node disease, and that is a pacing conversation rather than a drug one.

Differential

Normal Sinus Rhythm

The same trace above 60. Nothing but the rate separates them.

Junctional Escape Rhythm

Also slow, also regular, also narrow, but with no upright P before the QRS. Look in front of the complex, then behind it.

2:1 AV Block

Also slow and regular with a narrow QRS, and it is read as sinus bradycardia often. There are two P waves for every QRS, and the second one is easy to miss.

Sinus Arrest

Sinus bradycardia by mean rate, but produced by pauses rather than by uniform slowing. Measure several R-R intervals rather than one.

References

  1. Sinus Bradycardia — Life in the Fast Lane, ECG Library, 2024
  2. 2018 ACC/AHA/HRS Guideline on the Evaluation and Management of Patients With Bradycardia and Cardiac Conduction Delay — Circulation, 2019
  3. 2021 ESC Guidelines on cardiac pacing and cardiac resynchronization therapy — European Heart Journal, 2021