Mobitz Blocks are tricky.
Look at the ECGs below and work out if there is a Mobitz block. Then watch the 7 minute video below
An 80 yo woman presents to the emergency department with the complaint of feeling her legs give way. There has been no syncope, no injuries and the patient had no other clinical symptoms or signs, just the leg weakness. There was no headache, no palpitations, no chest pain, no shortness of breath, or abdominal pain ( review The SYNCOPE PLUS RULES).
An ECG was done as shown below, with an initial concern of ischaemia.
What does the ECG show?
Using the ECG in 20 seconds approach the following are obvious:
The changes on this ECG are not of classic morphology, so let's look at it a little more closely.
What does digoxin do?
Digoxin has a very narrow therapeutic index. It is used frequently and has positive inotropic and negative chronotropic effects. It decreases heart rate due to increased vagal activity, whilst shortening the action potential by increasing intracellular Calcium.
It is important to remember that the changes seen on ECG are due to the patient being on digoxin. They do not necessarily indicate toxicity.
T WAVE CHANGES
The T wave can be inverted or flattened or biphasic(usually in V4-6). It can look upright in its terminal portion however in most cases this is a U wave.
There is usually QT shortening
A 42 year old male presents to the Emergency Department with shortness of breath, palpitations and light headedness. This is a case from the literature(1).
His blood pressure at presentation is 85/65.
His initial ECG shows that he is in rapid atrial fibrillation.
It is decided to cardiovert this patient.
His cardiac tracing immediately post cardioversion with a biphasic defibrillator at 200J, with pads in the antero-posterior position is shown below. What does it show?
The tracing shows a Type I Brugada Pattern post cardioversion. It resolves after a few seconds.
What do we do with this? Is it significant?
Transient ST segment changes post cardioversion are well described. Their significance is uncertain.
Hypotheses for the ST segment changes include:
However, given that Brugada patterns predispose to ventricular arrhythmias, it may be prudent to monitor these patients for a period of time.
Read more on Brugada Syndrome and How to diagnose both Type I and Type II in the Cardiac Bootcamp Course.
1. Abdalla K et al Transient appearance of Brugada-like Type 1 electrocardiogram pattern immediately after biphasic synchronised electrical cardioversion for atrial fibrillation: a case series. European Heart Journal - Case Reports, Volume 3, Issue 4, December 2019, Pages 1–8
A 70 yo woman presents to the emergency department with a 3 month history of intermittent dizziness.
Her only past medical history is hypertension, for which she is on an ACE inhibitor. There are no other medications and she has no allergies.
On arrival the patient's vitals are BP of 190/95, pulse rate of 48bpm and sats of 99% on room air. She is seen by the registrar.
Her examination is normal. Dual heart sounds, nil extra sounds, normal respiratory exam, abdomen is soft and the neurological exam is normal. She is stable on her feet and walks around the department with no assistance.
Blood tests including FBC and UEC and Troponin are reported normal. The ECG is reported as normal.
The patient is to be discharged, when you review. What did the doctor miss?
To solve this case, we need to be suspicious as to why the patient has bradycardia, when they are not on a beta blocker.
The money is in the ECG. This is a MOBITZ II with a 2:1 Block
The problem with Mobitz II blocks like this is that they can deteriorate into a complete heart block.
The patient had a pacemaker inserted.
In last week's EMQA we spoke about a 2:1 block where the p waves were hidden in the T waves. These are not hidden.
CAUSES OF MOBITZ BLOCKS
A 70 yo male presents to the emergency department following a collapse at home. There is no prodrome and he does not remember the incident.
His ECG is shown below. What is the diagnosis?
There is also a prolonged QTc of about 500.
There is also a:
Cardiology argued that it was not. Read on to see why they were wrong.
What are the 3 Fascicles?
As the HIS Purkinje system enters the ventricular part of the heart it is composed of the:
If you want to find out about UNI/BI/TRIFASCICULAR Blocks as well as Complete and Incomplete Trifascicular Blocks become a Cardiac Bootcamp Course Member and become the expert.
Cardiac Bootcamp Course Members, go to the Fascicular Blocks page for more.
It costs less than 2 cups of coffee a week
Dr Peter Kas
A 54 yo male presents with left sided chest pain radiating to his jaw. He has vomited once.
His past medical history includes, Diabetes, Hypertension, an AMI (10 years ago) and Hypercholesterolemia.
His ECG is shown below:
This weeks ECG is contributed and discussed by Prof Louise Cullen, Emergency Physician Royal Brisbane and Women's Hospital and ACS researcher.
Answer the Questions below and then look at the case
A 40 yo male presents to the emergency department following an ingestion of a large amount of amphetamines. He is tachycardic and restless.
His vitals are:
HR 170 beats per minute in a narrow complex tachycardia
Sats 96% on RA
He is placed in an acute cubicle and monitoring is attached.
As an ECG is being done, the nurse calls for a doctor urgently 'He's gone into a wide complex tachycardia!" The ECG is shown below:
What is the rhythm?
(a) Ventricular Tachycardia
(b) SVT with RBBB
(d) Na channel Blockade
(e) Acute Myocardial Infarction
What favours Ventricular Tachycardia?
What favours SVT + RBBB?
How would you treat this patient?
When should Amiodarone not be given in an ECG like this?
He was shocked twice, with no resolution.
Why was this and what would you do next?
This is a great ECG.
Let's systematically go through it and apply the '120 CRAM' formula
Firstly we'll remind ourselves of the causes of wide complex tachycardia:
Remember these causes:
Let's work through it:
120: Is it faster than 120bpm and wider than 120ms but no too wide?
It's faster than 120bpm and wider- perhaps too wide. If the complexes are > 1 large square think hyperK.
In this case the K was 6.7mmol/L. We could stop there and treat with Calcium and add some bicarb and we could be done. But let's dig a little deeper and look at what else points to and against VT.
Beware giving the patient with hyperkalaemia Amiodarone as the K channels are already poisoned and the Amiodarone will poison the Na+ channels, which can result in asystole.
There is no concordance in the anterior leads, so this is against VT
R: R wave in aVR
There is no initial dominant R wave in avR, it's an RSR, so this is against VT
However if we look at aVR, there appears to be a terminal R wave consistent with Na channel blockade.
Does this look like a RBBB?
If we look at lead V1 , it has an rsR morphology, very similar to a RBBB. If it was VT it would have an Rsr morphology(remember the rabbit's ear). Plus we see that there is a rightward axis.
So so far it is looking like a hyperK + Na channel blockade + RBBB
A: AV dissociation
I can see p waves in V2. Is it dissociated? Hard to see that. Can you? It may be that the initial upstrokes in aVR are p waves.
Are there fusion or capture beats?
There may be some towards the end of the ECG, in the last few complexes, but I'm not sure.
Given that there is right bundle branch block morphology we look for 3 things:
I have presented this case in this way to you, to illustrate that applying the 120CRAM or any other algorithm can be confusing no matter how many you've done it before.
The following are important in this case:
What are the ECG effects of amphetamines?
Amphetamine overdose can result in significant ECG changes which include:
The patient had cardioversion attempted twice, with no effect, probably because this was not VT. The patient received calcium and bicarbonate.
The complexes narrowed.
So this was a Hyperkalaemic ECG with some Na channel blockade characteristics.
What would have happened if the patient had received Calcium early? It may have narrowed the complexes early.
A difficult case, but one that reinforces the approach we teach at Cardiac Bootcamp.
If at any time the patient is unstable, cardioversion is the option. If it isn't VT, nothing will happen
This week I looked at a recent paper on the predictive nature of ECG changes in those patient with Corona Virus
The paper reviewed was:
McCullough S.A et al. Electrocardiographic Findings in Coronavirus Disease-19: Insights on Mortality and Underlying Myocardial Processes. J Card Fail 2020 Vol 26;7:626-632
In this paper they looked at the prognostic significance given by the first ECG done in patients with COVID-19.
STUDY DESIGN: Retrospective Observational Cohort. In this study, the extraction of data from the electronic record was highly reliable.
PRIMARY OUTCOME: Mortality
STUDY SIZE: n= 756 over a 2 week period. Mortality occurred in 11.9%
It was interesting to note that ST Elevation was rare in this study. The ECG changes below, predicted a higher incidence of mortality.
Once again we see the ECG can give us a lot of information. In this case, beware these changes in a COVID patient, as they will predict a higher incidence of Mortality.
Isolated right ventricular infarction is rare, but it does occur in 30-50% of cases of inferior infarction. We need to think of the possibility of right ventricular infarction, or we can miss it.
The right ventricle is thin walled and is perfused throughout the cardiac cycle, explaining why it is less likely to infarct.
It is supplied by the right coronary artery, which also supplies the sinoatrial node and continues to supply the atrioventricular node in a large number of cases. This is the reason that we sometimes see bradycardia and blocks in patients with right coronary artery occlusion.
How do these patients present?Patients with right ventricular infarction will be pre-load sensitive, due to poor ventricular contractility. The result will be an increase in right ventricular diastolic pressures. Due to being preload dependant, there is a significant risk of severe hypotension when preload is decreased, such as occurs when we give nitrates.
Patients may present with hypotension, clear lung fields and distended neck veins. There may also be unexplained hypoxia, even with high levels of supplemental oxygen. This occurs due to the effects of right to left shunts via patent foramen oval or atrial septal defects becoming more pronounced as right sided pressures increase.
Some patients may present bradycardia due to the right coronary artery supplying the sinoatrial and atrioventricular nodes. These patients can become significantly compromised and require pacing.
Differential DiagnosisThere are many differentials, however some of the more important are:
The ECG below shows lead V4R( a single lead has been moved). There is ST elevation in the inferior leads( with ST elevation III>II) with reciprocal ST depression in I and aVL. There is also ST elevation in leads V1 and V2. The right sided lead V4R shows ST elevation of > 1mm.
ManagementPatients with right ventricular infarcts are preload dependent. Start initially with a fluid bolus such as 500ml of crystalloid. This may need to be repeated.
Remember NO NITRATES.
If the hypotension continues despite fluid loading consider inotropes. Dobutamine is the drug of choice as it improves cardiac index and right ventricular stroke volume.
Beware the patient who also has a left ventricular dysfunction. These patients will need support including after load reduction. This can be done with a nitroprusside infusion.
In the Wide Complex Rhythms part of the Course, I talk about the mimics of VT. However that's not all that can be mimicked.
If we don't recognised the mimic, we can actually do harm to the patient by giving treatment that isn't needed.
A holter monitor is done on a young patient who has complained of palpitations. His tracing is shown.
A diagnosis of VT is made. It's easy to be tricked. See the second ecg below.
Look at lead I below. It is not showing a wide complex. You can't have one lead refusing to show VT and all the others doing so. This is not a wide complex. This tracing was taken during a time when the patient was playing a video game on their phone. The tapping came produced this complex.
A similar interference pattern can occur secondary to tremor, or rigors, or someone just tapping on the lead.
Below is another case.
A 35 yo male with known Cardiomyopathy presents to the ED with chest pain.
The diagnosis of atrial flutter is made by the registrar, after seeing the rhythm on the monitor.
He is planning for definitive treatment; in this case cardioversion. That's another discussion. (I wouldn't necessarily cardiovert atrial flutter on presentation.)
An ECG is done.
Is this atrial flutter?
What else could it be if it isn't flutter?
See the ECG below:
This is nothing more than artefact. If you look closely at the ECG you can see that the patient’s underlying rhythm. The tall QRS complexes (well seen in V4-6), are the patient's underlying rhythm. There is left ventricular hypertrophy due to the patient’s cardiomyopathy. The waveforms in-between these, are simply artefact, just noise. In this case they are created due to the patients underlying tremor.
The 12 lead ECG was seen and the diagnosis of flutter was still entertained by the registrar.
If we look at this ECG, we can see where I’ve circled the complexes in lead III.
You can’t have atrial flutter in every lead, but lead III refuses to go into flutter. It’s artefact created by patient tremor and movement. It was easily reproduced by my tapping on the leads.
Now even though this wasn’t flutter we still needed to sort out the chest pain with serial Troponins.