Life in the Slow Lane

Slim slow slider
Horse you ride white as snow
Tell it everywhere you go
— Slim Slow Slider by Van Morrison from the Astral Weeks album

These cases were seen during the last two weeks, and have a common theme of a slow heart rate.

Fifty two year old man admitted to the Short Stay Unit in the ED because of severe lower back pain. He had required regular doses of oxycodone to control the pain


+ Describe the main ECG findings

Why was this ECG done? Does every person (in this case a healthy 52 year man with no medical problems) need an ECG if they present with severe acute back pain that has typical features of musculoskeletal pain? Not unless there is some abnormality that might be due to underlying cardiovascular disease. In this case the patient had a radial pulse of about 50 beats per minute.

What are the main ECG findings?

Figure 2

The rhythm strip (Figure-2) shows sinus rhythm with slight variation in the R-R intervals (1280 to 1440 msec) that is consistent with sinus arrhythmia. Sinus bradycardia is present, with a heart rate between 42 - 47 beats per minute.

The morphology of the QRS complexes is normal, but some of the QRS complexes in the frontal leads have a low amplitude (low voltage if an alternative term). Figure 2 shows that four of the frontal leads have a QRS amplitude of 5.5 mm (5.5 mV).

Does this fit the criteria for low QRS voltages? Low electrocardiographic QRS voltage (LQRSV) is defined as a decreased zenith-to-nadir QRS amplitude in both the frontal leads and the precordial leads that is

  • less than 0.5 mV (5 mm) in all the frontal leads
  • less than 1.0 mV (10 mm) in all the precordial leads

The ECG of R-0012 does not meet the criteria for LQRSV.

The frontal plane axis, the PR interval, the QRS duration and the QT intervals are all normal. The QRS complexes have normal morphology, and the ST segment and the T waves are normal.

Final ECG diagnosis:

  • Normal ECG with sinus bradycardia and sinus arrhythmia
  • Non specific finding of low amplitude QRS complexes in most of the frontal leads.

What could be the cause of the sinus bradycardia? The patient is not an extremely fit person. There is no history of cardiac disease or syncope, the cardiovascular examination is normal, and there are no ECG features of conduction disorder. The patient is not on any cardiac medications that could explain the bradycardia. We are left with two possibilities:

  • The ongoing and not fully controlled back pain has caused an increased vagotonia.
  • Could the regular doses of endone that the patient has received affect the heart rate?

Opioid receptors are present in cardiac cells, and experiments using spontaneously beating isolated rat hearts have found that stimulation of δ- and κ-receptor agonists reduced heart rate and contractility when directly added into the perfusate (Source: Wei Huang. 2013 MD Thesis Direct functional effects of opioid agonists on the isolated perfused rat heart)

Key Points

  • Possible association between opioid use and the sinus bradycardia in this case
  • Diagnostic criteria for low QRS voltage (LQRSV) complexes in ECGs

This 65 year old man presented with dizziness for investigation. He had a past history of Human Immunodeficiency Virus infection and thyroidectomy. Examination of the nervous system was normal, apart from the observation that he was a vague historian. The following blood tests results from 30 months ago were normal: electrolytes, urea and creatinine concentration; calcium & phosphate concentration; full blood examination; thyroid function tests.
Figure_1 shows the ECG taken on arrival.


The patient was admitted to the Short Stay Ward for cardiac monitoring overnight, after having a brain CTthat was normal.

+ Describe the ECG changes (the patient does not have chest discomfort, and a serum troponin concentration on arrival is normal). There are no previous ECGs for comparison.

The main ECG changes in R-0013 are

  • Sinus rhythm with a heart rate of about 52 beats per minute

  • Prolonged PR interval

  • T wave flattening in the anterolateral leads

  • Q waves in Leads V1 to V3 and I mm of ST elevation in Lead V2 and Lead V3

  • The QRS complexes in Lead I, Lead III, Lead aVL and Lead aVF have a low amplitude (5 mm [0.5 mV] or less). The QRS amplitude in Leads V1, V4 and V6 have a low amplitude (10 mm or less)

+ Are any other investigations indicated before discharging the patient?

Additional tests before discharge would be

  • CXR (this showed slight cardiomegaly)
  • Thyroid function tests. The results of the thyroid function tests were: TSH of 178.2 mIU/L (normal 0.4-4.0 mIU/L). A free thyroxine level of < 5.2 pmol/L (normal 10-25 pmol/L). The patient is hypothyroid

  • A bedside echocardiogram could be done (looking for a pericardial effusion) once the results of the thyroid blood tests are known.

See the section on Thyroid Disease and the ECG in the Nuts & Bolts of the ECG for more information

This 80 year old woman came by ambulance to the ED because of chest discomfort. This began at rest and involved the lower retrosternal and epigastric regions. The discomfort was constant, mild in severity and did not radiate. She had associated symptoms of dyspnoea and palpitations. The discomfort was not relieved by a GTN spray, and lasted about one and three quarter hours before being relieved by a GTN patch and intranasal fentanyl.

She has a history of a acute myocardial infarct 22 years ago, and is on long term clopidogrel. 

Her ECG taken on admission is shown in Figure_3.

Figure 3

+ Describe the main findings in the ECG

The obvious ECG findings are:

  • Sinus rhythm with a heart rate of about 62 beats per minute
  • Left anterior hemiblock
  • Flattened T waves in Leads V5 -V6
  • Deep S wave in the precordial leads, with most of the complexes having a rS morphology.
  • The less obvious but significant finding is the shape of the QRS complex in Lead V2 compared to the shape in Lead V1 and Lead V3. Lead V2 has a smaller amplitude and a different shape (RS) than the rS shape in Lead V1 and Lead V3. This transition cannot be explained by the normal progression of ventricular depolarization, but suggests a misplaced chest lead. This is confirmed by looking at a ECG taken 3 months ago (Figure_2).

Figure 2

Key Point

Check the progression of the QRS morphology of the complexes in the precordial leads. An unusual or out of sequence morphology in a single lead can be due to a misplaced chest lead. If this is the case repeat the ECG or compare it to a previous ECG.

This 70 year old man has a past history of insulin dependent diabetes and of triple vessel coronary artery disease. He has been transferred from another hospital for admission to the Coronary Care Unit. He is on an isoprenaline infusion.

Figure 4

+ Describe the changes in the ECG taken an arrival

Figure 2 shows the rhythm strip from R_0015.

Figure 2

Atrial rhythm and rate

The start of clearly visible P wave (1 - 5 and 8 - 15) is marked by a solid blue arrow. The interval between these visible P waves is 640 msec, and this interval is used to mark the place where P waves between wave 5 and and wave 8 should appear but are not seen. There are two such waves (6 and 7), each marked by a dotted arrow. Wave 6 is obscured by the end of the T wave of the third ventricular complex, and wave 7 is buried in the QRS of the fourth ventricular complex. The atrial rhythm is sinus, with a atrial rate of about 94 beats per minute

Ventricular rate and rhythm

The QRS complexes are numbered (1 - 9), and the R-R interval in shown in msec. The R-R interval between ventricular complexes 3 and 9 is regular, with a duration of 1080 msec. This corresponds to a ventricular rate of about 56 beats per minute. There is no constant relation between the P waves and the ventricular complexes (apart from ventricular beat 2), so atrioventricular dissociation is present. Ventricular beat 2 has an earlier onset (R-R interval between 1 and 2 is 920 msec) and is followed by a longer R-R interval (of 1200 msec) between ventricular beats 2 and 3. Ventricular beat 2 is narrower and has a different QRS shape than the other ventricular beats. Ventricular beat 2 is thus a capture beat The QRS complexes have a left bundle branch block (LBBB) morphology, with normal axis and a prolonged QT interval. The ST-T changes that are present are (probably) secondary to the LBBB. There is 1 mm ST elevation in Lead V1 and Lead V2. The "typical" LBBB morphology of the QRS complexes suggests a nodal origin of the ventricular rhythm rather than a more distal (idioventricular) origin. The usual ventricular rate of a nodal escape rhythm is 40 - 60 beats per minute, with faster rates called "accelerated nodal (junctional) rhythm". The ventricular rate in this case is near the upper limit of normal for a nodal escape rhythm

Summary of ECG findings

  • Atrial rhythm (sinus) at a rate of about 94 beats per minute
  • Atrioventricular dissociation (with one ventricular capture beat)
  • Nodal (junctional) rhythm at a rate of about 56 beats per minute
  • Left bundle branch block
  • Prolonged QT interval

This 82 year old man presented with chest pain. 

+ Describe the changes in the ECG taken on arrival at 0204 and the ECG taken at 0734

Figure 3

Figure 3 is the rhythm strip of R0016_A. The main findings are: The horizontal green line marks an interval of 3 seconds. There are 3 ventricular complexes in this interval, so the ventricular rate is 3 x 15 beats per minute i.e. 60 beats per minute. The QRS complexes are narrow with a width of 0.08 seconds. The complexes have a small notch at the end of the downstroke of the R wave, but the notch is also seen in Lead 2 in the second ECG when the patient is in sinus rhythm. The notch is thus not a retrograde P wave P waves are not seen (but see below) The R-R intervals between the ventricular complexes vary, which raises the possibility of atrial fibrillation. The small (low amplitude), irregular waves (fibrillation or f waves) in the isoelectric line that are usually seen in atrial fibrillation are not present. The repetitive pattern of the ventricular beats would not occur in atrial fibrillation.

Rhythm strip diagnosis: Junctional (nodal) rhythm with a ventricular rate that is at the upper end of the range seen in a junctional escape rhythm or the lower end of the range seen in an accelerated junctional rhythm.

Although there are no obvious P waves in the rhythm strip from R0016A, a small downward deflection is seen after the T wave of beats 1, 4 and 7. This marked by a red asterisk in Figure_4. This might be a retrograde P wave.

Figure 4

A laddergram analysis (Figure_5) shows a possible mechanism that would link the junctional rhythm and retrograde atrial activation.

Figure 5

Laddergram diagnosis Junctional rhythm with a bigeminal pattern where every second junctional impulse conducts to the atria, inscribing a inverted P wave. The atrial impulse associated with this P wave then travels in an antegrade direction to activate the ventricle. This produces a repetitive sequence where the R-R intervals between beats 1 and 4 are 800, 1320 and 1400 msec, the intervals between beats 4 and 7 are 820, 1360 and 1400 msec and between beats 7 and 8 is 840 msec. The R-R interval between beats 3 and 4 and between beats 5 and 6 gives us the underlying rate of the junctional rhythm as 43 beats per minute.

The second ECG (R0016B) was taken after a period of monitoring, without any treatment. There is sinus rhythm with a rate of 79 beats per minute, a prolonged PR interval of 0.24 seconds and 1-2 mm of ST elevation in Leads V2 and V3