Saturday 31 July 2021

The definition of type 2 MI is21 “myocardial infarction secondary to ischaemia due to either increased oxygen demand or decreased supply, e.g. coronary artery spasm, coronary embolism, anaemia, arrhythmias, hypertension or hypotension”

https://litfl.com/premature-ventricular-complex-pvc-ecg-library/

ventricular bigeminy: Premature Ventricular Complex (PVC)

Ed Burns and Robert Buttner
Jun 2, 2021

ECG Library Homepage

A premature ventricular complex (PVC) is a premature beat arising from an ectopic focus within the ventricles. AKA: ventricular ectopics, ventricular extrasystoles, ventricular premature beats, ventricular premature depolarisations.

ECG features of PVCs

Broad QRS complex (≥ 120 ms) with abnormal morphology
Premature — i.e. occurs earlier than would be expected for the next sinus impulse
Discordant ST segment and T wave changes.
Usually followed by a full compensatory pause
Retrograde capture of the atria may or may not occur

Origin of Ectopic Beats

Groups of pacemaker cells throughout the conducting system are capable of spontaneous depolarisation
The rate of depolarisation decreases from top to bottom: fastest at the sinoatrial node; slowest within the ventricles
Ectopic impulses from subsidiary pacemakers are normally suppressed by more rapid impulses from above
However, if an ectopic focus depolarises early enough — prior to the arrival of the next sinus impulse — it may “capture” the ventricles, producing a premature contraction
Premature contractions (“ectopics”) are classified by their origin — atrial (PACs), junctional (PJCs) or ventricular (PVCs)

Electrophysiology of Ventricular Ectopics

Ectopic firing of a focus within the ventricles bypasses the His-Purkinje system and depolarises the ventricles directly
This disrupts the normal sequence of cardiac activation, leading to asynchronous activation of the two ventricles
The consequent interventricular conduction delay produces QRS complexes with prolonged duration and abnormal morphology

Discordance

Appropriate discordance describes a pattern of repolarisation abnormality (typically seen with left bundle branch block, paced rhythms, VT) in which the ST segment and T wave are directed opposite to the main vector of the QRS complex. Because there is abnormal depolarisation, there is subsequent abnormal repolarisation which is discordant:

ST depression and T wave inversion in leads with a dominant R wave
ST elevation with upright T waves in leads with a dominant S wave

With a full compensatory pause, the next normal beat arrives after an interval that is equal to double the preceding R-R interval

Retrograde capture describes the process whereby the ectopic impulse is conducted retrogradely through the AV node, producing atrial depolarisation. This is visible on the ECG as an inverted P wave (“retrograde P wave“), usually occurring after the QRS complex.

PVCs are said to be “frequent” if there are more than 5 PVCs per minute on the routine ECG, or more than 10-30 per hour during ambulatory monitoring.

Classification

PVCs may be either:

Unifocal — arising from a single ectopic focus; each PVC is identical
Multifocal — arising from two or more ectopic foci; multiple QRS morphologies

The origin of each PVC can be discerned from the QRS morphology:

PVCs arising from the right ventricle have a left bundle branch block morphology (dominant S wave in V1)
PVCs arising from the left ventricle have a right bundle branch block morphology (dominant R wave in V1)

PVCs often occur in repeating patterns:

Bigeminy — every other beat is a PVC
Trigeminy — every third beat is a PVC
Quadrigeminy — every fourth beat is a PVC
Couplet — two consecutive PVCs
NSVT — between three and thirty consecutive PVCs (see below)

Clinical Significance

PVCs are a normal electrophysiological phenomenon not usually requiring investigation or treatment
Frequent PVCs may cause palpitations and a sense of the heart “skipping a beat”
In patients with underlying predispositions (e.g. ischaemic heart disease, WPW), a PVC may trigger the onset of a re-entrant tachydysrhythmia — e.g. VT, AVNRT, AVRT

Frequent PVCs are usually benign, except in the context of an prolonged QTc, when they may predispose to malignant ventricular arrhythmias such as Torsades de Pointes by causing “R on T” phenomenon

Causes

Frequent or symptomatic PVCs may be due to:

Anxiety
Sympathomimetics
Beta-agonists
Excess caffeine
Hypokalaemia
Hypomagnesaemia
Digoxin toxicity
Myocardial ischemia

Example ECGs

Multifocal PVCs

ECG Multifocal Premature Ventricular Complex (PVC)

Sinus rhythm with PVCs of two different morphologies (arrows)
Note the appropriately discordant ST segments / T waves
The pause surrounding the PVC is equal to double the preceding R-R interval (= a full compensatory pause)

Ventricular bigeminy

ECG Premature Ventricular Complex (PVC) Bigeminy

Premature Ventricular Complex (PVC) bigeminy

Ventricular quadrigeminy

ECG Premature Ventricular Complex (PVC) Quadrigeminy

PVC pairs (couplets)

Non-sustained VT (NSVT)

When is a PVC not a PVC?

Definitions vary regarding 3 or more PVCs
Some authors define three PVCs as a triplet of PVCs; whilst others describe this as a ‘short burst of VT’; but more commonly as NSVT
A consensus definition would be: 3-30 consecutive PVCs with a rate >100bpm described as non-sustained VT (ventricular rhythm if rate <100bpm)

Friday 30 July 2021

lbbb vs rbbb

NOVEMBER 1, 2013

Bundle Branch Blocks: 101

Written by Salim Rezaie REBEL EM Medical Category: Cardiovascular 0 Comments

Recently, I have been asked by several students at my home institution (UTHSC at San Antonio) to help them understand bundle branch blocks. This is different than some of my usual posts because it is meant to be more educational than evidence based. So here we go. The normal conduction system of the healthy heart is shown to the right. If there is a delay or block in the left or right bundle, depolarization will take longer to occur. Therefore we get a widened QRS (>0.12 sec or >3 small boxes).

Conceptual Tip

One thing to remember to make this easier on yourself is that an “S Wave,” essentially means depolarization is going away from something and an “R Wave,” means depolarization is going toward something. As you continue to read this post just remember S = Away and R = Toward.

Is it LBBB or RBBB?

Once you have identified that your QRS is wide go to lead V1. If the “terminal force” of the QRS is above the baseline (big R wave) you have a RBBB. If the “terminal force” of the QRS is below the baseline (big S wave) you have a LBBB.

RBBB and LBBB

Image from ECGPedia.org

Why does a LBBB have a “big S Wave” and RBBB a “big R Wave” in lead V1?

In RBBB, the last depolarization to occur is in the right ventricle therefore the left ventricle depolarizes first, which means the conduction is moving toward V1 (Left to Right).
In LBBB, the last depolarization to occur is in the left ventricle therefore the right ventricle depolarizes first, which means the conduction is moving away from V1 (Right to Left).
Remember the right side of the heart sits closer to the chest wall than the left side of the heart

Are there more specific criteria for RBBB and LBBB?

RBBB
- QRS duration >0.12 seconds
- Slurred S wave in lead I, aVL, V5, and V6 (Depolarization moving away from these leads)
- RSR’ in V1 and V2 with R’ > R (Depolarization moving toward these leads)

Normal RBBB

ECG from Dr. Smith’s ECG Blog

LBBB
- QRS duration >0.12 seconds
- Broad monomorphic R waves in I, aVL, V5, and V6 (Depolarization moving toward these leads)
- Broad, dominant, monomorphic S wave in V1 and V2 (Depolarization moving away from these leads)

LBBB

ECG from Dr. Smith’s EGG Blog

Left bundle with anterior and posterior fascicle

I wish I could say that it is just that easy, but it gets more complicated. The left bundle actually has an anterior and a posterior fascicle. This changes the morphology and the axis of the ECG. I will try and go through this to help simplify the ECG as we did with LBBB and RBBB.

Conduction System of the Heart

Left anterior fascicular block (LAFB)

Lets start with LAFB. If the left anterior fascicle is blocked, then depolarization in the left ventricle will go toward the lateral leads (I and aVL) and away from the inferior leads (II, III, and aVF). This means you would expect to see a bigger R wave in leads I and aVL and a bigger S wave in leads II, III, and aVF.

What are the criteria for LAFB?

Slightly prolonged QRS duration (Not quite 120 msec or < 3 small boxes)
Left axis deviation
qR complex in leads I and aVL (Depolarization going towards these leads)
rS complex in leads II, III, and aVF (Depolarization going away from these leads)

LAFB

Left Posterior Fascicular Block (LPFB)

Lets now move on to LPFB. In general it is rare to find LPFB in isolation, because it is typically seen with RBBB. For the sake of explanation, if the posterior fascicle is blocked in isolation, then depolarization in the left ventricle will go toward the inferior leads (II, III, and aVF) and away from the lateral leads (I and aVL). This means you would expect to see a bigger R wave in leads II, III, and aVF and a bigger S wave in leads I and aVL.

What are the criteria for LPFB?

Slightly prolonged QRS duration (Not quite 120 msec or < 3 small boxes)
Right axis deviation
qR complex in leads II, III, and aVF (Depolarization going towards these leads)
rS complex in leads I and aVL (Depolarization going away from these leads)
Absence of right ventricular hypertrophy or prior lateral myocardial infarction

LPFB

Hopefully, this helps simplify bundle branch blocks and how to read them on ECGs. Just remember:

S wave = depolarization away from leads
R wave = depolarization towards leads

Cite this article as: Salim Rezaie, "Bundle Branch Blocks: 101", REBEL EM blog, November 1, 2013. Available at: https://rebelem.com/bundle-branch-blocks101/.