A bradycardia can dramatically decrease someone's cardiac output, thus a bradycardic patient may present with syncopal events, signs of heart failure or even an ischaemic event. Most bradycardias have a reversible cause e.g. iatrogenic or the result of an acute illness, but it is important to be able to identify a primary rhythm disturbance as the cause i.e. a bradyarrhythmia. Among our aging population these are increasingly seen, as senile and ischaemic changes frequently affect the heart's conduction system.
Classically a bradycardia is a heart rate below 60bpm, but some textbooks refer to absolute bradycardia as a heart rate below 40bpm. However it is probably more useful to gauge if the heart rate represents a relative bradycardia for that individual patient, by taking into account their previous heart rate, their haemodynamic status and concurrent illness etc.
Initially, assess the bradycardic patient using an ABCDE approach. it is important to assess whether a patient requires emergency management of their bradycardia e.g. atropine. To do this you must decide whether they have any signs of compromise. The managment of compromised patients will be covered in the acute section of the website, but below is an algorthm adapted from the resus council.
Signs of compromise:
Bradycardias caused by the SA node are very common. They are either caused by extrinsic factors affecting SA node function e.g. drugs, causing a sinus bradycardia, or by intrinsic dysfunction of the SA node i.e sick sinus syndrome.
Although not strictly a bradyarrhythmia, because the ECG morphology is normal, sinus bradycardia is an important differential for bradyarrhythmias and is extremely common.
Remember it is normal for people like athletes to have a sinus bradycardia at rest due to their increased vagal tone inhibiting the natural rate of the SA node. The intrinsic rate being 60-100bpm.
SSS is intrinsic dysfunction of the SA node. It is increasingly common with age and most often related to degenerative fibrotic changes within the node. SSS gives rise to bradyarrhythmias with characteristic ECG patterns. The main disturbances are SA Arrest, SA Block and Tachy-Brady syndromes.
SA arrest, otherwise known as a sinus pause, is caused by failure (usually transient) of the sino-atrial node to depolarise, therefore the atria and ventricles fail to depolarise and there is an absent p:QRS wave on the ECG. Electrical activity resumes either when the SA node resumes normal activity or when an ectopic pacemaker takes over.
Sinus Arrest vs. Sinus Block
A sinus arrest is defined as absence of normal p-waves on the ECG for more than 2 seconds. Additionally, the interval between the last normal p-wave and the next normal p-wave may not be a multiple of the normal p:p interval, because this would suggest the dropped p:QRS is due to a sinus block, not a sinus arrest. (see ECGs below)
In SA block the SA node does depolarise, but the impulse conduction to the atria is affected. Discussion of the different types of SA block is beyond the scope of medical finals. Suffice to say that, as with AV block, there are 3 degrees of block:
Tachy-brady syndrome is caused by the association between SA node dysfunction and tachyarrhythmias (usually supraventricular). Patients typically experience a run of tachyarrhythmia followed by a period of bradycardia. It is common for the 2 to coexist, with 50% of those with SA node bradycardia also experiencing tachyarrhythmias. There are numerous mechanisms by which this phenomenon can occur (knowing these is beyond the scope of medical finals). For example:
AV node bradycardias are classified as disorders of rhythm because the dysfunction of the AV node changes the normal ECG morphology. Conduction through the AV node can either be delayed (1st degree heart block), partially blocked (2nd degree heart block) or completely blocked (3rd degree heart block). The pathology occurs either within the AV node itself or just beyond it, within the His-Purkinje conduction system.
1st degree AV node block is simply delayed conduction through, or near, the AV node. This is usually asymptomatic and diagnosed on ECG where the PR interval will be more than 5 small squares (0.2s) on a standard strip. A narrow QRS complex indicates that the block is likely to be within the AV node and a wide QRS complex indicates a His-Purkinje block.
1st degree heart block rarely causes a bradycardia, but can lead to higher levels to AV nodal block.
If the patient is asymptomatic, no treatment or follow-up is needed. For symptomatic patients consider pacemaker insertion.
2nd degree AV node block is partial conduction through, or around, the AV node i.e. some p waves are followed by a QRS complex and some are not. Patients may be asymptomatic or may have palpitations and be aware of dropped beats. There are 2 types of 2nd degree AV node block; Mobitz type 1 (Wenkebach) and Mobitz type 2. These are prognostically very different.
The PR interval progressively lengthens with each beat until a a wave is not followed by a QRS complex. This will continue as a cycle. The primary defect is usually conduction within the AV node itself and often vagally mediated.
Higher levels of block are unlikey to occur with Mobitz 1. No treatment or follow-up is usually required.
Impulses intermittently fail to be conducted, without prolongation of the PR interval. This may occur in a regular pattern e.g. every third p wave is not followed by a QRS complex; known as a 3:1 block. The block is usually within the bundle of His and can lead to widened QRS complexes.
Mobitz 2 is likely to progress to 3rd degree heart block, subsequently a permanent pacemaker is almost always indicated for these patients. Widened QRS complexes indicate a worse prognosis.
3rd degree heart block is where there is complete dissociation between atrial and ventricular depolarisations because all impulses from the atria are blocked by the AV node. Ventricular depolarisations occur as a result of an escape rhythm. Escape rhythms are initiated by one of the heart's back-up pacemakers. If the QRS complexes are narrow on the ECG then the escape rhythm is being initiated from the AV node itself. If the QRSs are wide then the escape rhythm is being initiated further down the conducting system or by an ectopic ventricular pacemaker. The ECG will show no pattern between the p waves and the QRS complexes. The patient will be bradycardic as a result of the escape rhythm which is usually 30-40bpm.
Those with 3rd degree AV block are usually symptomatic from their reduced cardiac output. Syncopal attacks are common; known as Morgagni-Adams-Stokes (MAS) attacks. As a result, most people will need a permanent pacemaker (unless it is expected to swiftly resolve due to a treatable cause).
Bundle branch blocks are very common ECG abnormalities and although they don't in themselves manifest as a bradycardia they are caused by slowed conduction through the ventricular system. They can also lead to higher levels of block which can cause a bradycardia.
Normal ventricular depolarisation occurs down the bundle of His and then through the right and left bundles. (The septal area of the heart depolarises from left to right). When one of the main bundles is blocked, depolarisation to that side of the heart occurs via the other bundle and is transmitted by non-specialised ventricular tissue in between. This slows the whole process down leading to a wide QRS complex on the ECG. This makes bundle branch blocks very easy to recognise (working out what type it is is a little trickier).
RBBB almost always has a pathological cause. Causes include:
NB: In RBBB ST segment abmormalities are common in V1/V2, so it is often difficult to comment on ischaemic changes when analysing the ECG.
The above changes may be difficult to pick out. Remembering the word MARROW may help you to identify the changes.
The left bundle branch is supplied by both the right and left coronary arteries. Therefore LBBB is common in those with extensive coronary artery disease and can be the consequence of an acute anterior MI. It is also seen in those with hypertension and cardiomyopathy.
NB: In LBBB the ST segments displace in the opposite direction to the (overall) direction of the preceeding QRS complex. Again, making it difficult to analyse the ECG for ischaemic change. Left axis deviation is commonly associated with LBBB.
The above changes may be difficult to pick out. Remembering the word WILLIAM may help you to identify the changes.
The left bundle branch splits into 2 fascicles: the anterior and posterior fascicles. When conduction through one of the fascicles is blocked it is called an anterior or posterior hemiblock, respectively. Left anterior hemiblock is more common and causes left axis deviation on the ECG. Left posterior hemiblock causes right axis deviation on the ECG.
This is a combination of right bundle branch block and either left anterior or left posterior hemiblock. The ECG will show RBBB with either left (anterior hemiblock) or right (posterior hemiblock) axis deviation.
This is when bifascicular block is associated with 1st degree heart block.
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