Understanding ECGs: bradycardias--fit and fitting
In the fourth article in our series Dominic Cox and Hamish Dougall look at bradycardias--their diagnosis, significance, and management
Symptoms from slowing of the heart can be very varied, from sudden death, recurrent syncope, and epileptic-type fits, to much milder symptoms, such as lethargy, breathlessness, etc. The history can be very revealing, but can also be very unreliable in those patients who truly lose consciousness. Some bradycardias are only intermittent problems with bothersome recurrent blackouts but no abnormality found after many years of medical investigation. Getting evidence of an intermittent problem can be very difficult.
Bradycardia is "slow" cardiac rhythm and results from either a failure of initiation of the heart beat or failure of passage of this electrical message through the heart--that is, normal sinus node "spark plug" activity is disturbed or there is interruption of the passage of this activity to tell the pump to work. This second type of failure usually occurs at the atrioventricular (AV) node.
The intrinsic rate of the sinoatrial (SA) node, which controls the heart rate in normal circumstances, is 60 to 70 beats per minute, and a bradycardia is defined as a pulse rate of <60 beats per minute. Such a rate may be physiological (and therefore acceptable) in athletes, young people, or during sleep, but it can be of profound clinical significance resulting from acute myocardial infarction, sick sinus syndrome, or from a variety of different drugs--for example, beta blockers. Several non-cardiac disorders, such as hypothyroidism, hypothermia, jaundice, and raised intracranial pressure can also cause sinus bradycardia.
Identifying the important different types of bradycardias is relatively straightforward and will be considered in turn: sick sinus syndrome (sinoatrial disease); carotid sinus hypersensitivity; vasovagal syndrome; AV heart block; agonal rhythm; asystole.
Likewise the treatment options are few in number and basically consist of removing or treating the underlying cause: (a) resuscitation with drugs to stop the heart slowing (atropine); (b) drugs to speed up the heart (isoprenaline); (c) pacing the heart electrically.
The first three conditions are predominantly problems with the SA node or its innervation.
ECG 1: Patient who has gone into slow atrial fibrillation
ECG 2: This ECG of a young patient undergoing cartoid sinus massage shows profound slowing of the P wave rate. There is lengthening of the PR interval and then complete loss of ventricular activity for over 3 and a half seconds
ECG 3: First degree heart block: a constant prolonged PR interval
Sick sinus syndrome (SSS)
This is common in the elderly and is usually caused by idiopathic degeneration of the SA nodal cells. Sinoatrial disease may be associated with coronary artery disease, particularly that involving the right coronary artery, although many of these patients have normal coronary arteries. It causes bradycardia that can be profound enough to cause arrest; SA block; or supraventricular tachycardia (SVT) alternating with bradycardia ("tachy-brady syndrome").
Patients may be completely asymptomatic, in which case usually no treatment is indicated. They can present with symptomatic bradycardia, dizziness, or syncope. The diagnosis is from 12 lead or 24 hour ambulatory ECG recording and, importantly, demonstrating a correlation between periods of bradycardia, or sinus pauses, and symptoms. It is accepted that a pause of over three seconds is significant. (ECG 1)
Normal PR interval (because this is an SA node, not an AV node, problem). Every P wave is followed by a normal QRS complex (unless dual pathology), but there are periods when interval between P waves (P-P interval) is prolonged.
Treatment: Removal of extrinsic causes of bradycardia and/or permanent pacemaker (PPM) implantation. Note that in the tachy-brady syndrome once a PPM has been implanted medications which would normally slow the intrinsic cardiac rate can then be used to control the SVT--for example, beta blockers.
Carotid sinus hypersensitivity
Similar symptoms to SSS can occur due to a hypersensitive carotid sinus reflex. It is diagnosed by finding either a sinus pause or of AV block greater than three seconds in response to five seconds of carotid sinus massage. Again where an association is made between symptoms and ECG findings then PPM is indicated.
Note that carotid sinus massage affects both SA and AV nodes, therefore as well as a sinus bradycardia the PR interval can also be prolonged resulting in AV block [ECG2]
Vasovagal syndrome
This is a common condition, particularly in younger people, and a more malignant variety is recognised in the more elderly. This vagally mediated bradycardia can be treated by PPM.
ECG 4: Mobitz type I or Wenckebach block
ECG 5: Mobitz type II second degree atrioventricular (2:1)
AV heart block
AV heart block is divided into first, second, and third degree AV blocks, which as the names suggest, involve a problem at the AV node!
All three variants involve the association between the P wave and the QRS complex. Because the problem is not with the SA node or the ventricular polarisation itself, then both the P wave and QRS complex commonly look normal. It is the association between the two that is seen to be different, and this is because they are connected via the AV node. Causes of AV block are shown in the box.
Causes of AV block
- Acute myocardial infarction or ischaemia
- Drugs--beta blockers, verapamil, digoxin, Class I antiarrhythmics
- Infection--diphtheria, rheumatic fever, endocarditis, Lyme disease
- Idiopathic fibrosis of the conducting system
- Infiltration--sarcoidosis, syphilis, scleroderma, tumour, calcific aortic stenosis
First degree AV block
The PR interval is prolonged (>0.20 sec) but constant (ECG3).This does not produce any symptoms and does not require any active treatment.
Second degree AV block
There are two types of second degree block:
Möbitz type I (also known as Wenckebach) has a progressively lengthening PR interval that eventually drops a QRS complex and starts over with a progressively lengthening PR interval before dropping a QRS complex again--need I go on? (ECG 4) This is normally associated with a reliable subsidiary pacemaker and a lower chance of progressing third degree block. Pacemaker implantation is not mandatory without evidence of correlated symptoms or undue bradycardia.
Möbitz type II is different in that the PR interval is constant but occasionally a P wave is not conducted through the AV node and is therefore not followed by a QRS complex--that is, there is a "dropped beat." Regular non-conducted P waves may result in a high degree block. If only every second or third P wave is followed by a QRS complex then there is said to be 2:1 block or 3:1 block respectively. (ECG 5) Type II AV block usually indicates an extensive infranodal abnormality and therefore, except in the context of an acutely reversible condition, requires a permanent pacemaker.
Third degree AV block (complete heart block)
In this, there is regular firing of the SA node giving regular P waves. The P waves, however, do not get through the "broken" AV node. Most cardiac tissue can produce some spontaneous activity. The lonely ventricle now electrically separated from the atrium usually produces its own slow heart rhythm. Often this comes from near the start of the His Purkinje system, leading to a narrow normal complex QRS. If the complex arises more distally then the complex cannot be propagated in the normal manner. It therefore takes longer to transmit across the ventricle and therefore the QRS complex looks wider. (ECG 6) A permanent pacemaker is essential, even if asymptomatic, as there is a risk of sudden death.
ECG 6: Third degree or complete heart block. There is clearly no association between the frequent P waves and narrow complex ventricular rhythm.
ECG 7: Agonal rhythm
Agonal rhythm
This is a slow, irregular rhythm with wide ventricular complexes of varying morphology, which is often seen during the later stages of unsuccessful resuscitation attempts as the heart dies. The complexes become progressively broader before all recognisable activity is lost. (ECG 7)
Pacemakers
Pacemakers treat all types of bradycardia and also interfere with and abort many tachycardias. They can also be used to reco-ordinate ventricular function in patients with heart failure and damaged electrical conducting systems. Most pacemakers listen to the heart's own rhythm and leave things alone as long as things are working properly. If the heart beat changes they then step in to stimulate the heart appropriately.
To do this the pacemaker is comprised of three parts: the wires, the battery, and the computing system. Most wires or leads are placed inside the heart via the subclavian or other vein. Sometimes leads are placed on the surface of the heart (epicardial) via opening the chest in a more invasive procedure. These wires are the permanent part of the system. The battery and computer are inside a can which attaches to the leads.
Asystole
This is not really a bradycardia, rather a complete cessation of both atrial and ventricular activity. If the ECG shows asystole and the patient is speaking to you then you need to check that your leads are properly attached. If there are persisting P waves but no ventricular activity then it is called ventricular standstill.
The emergency treatment of most bradycardias is atropine, a pacemaker, or sympathomimetic drugs, such as adrenaline or isoprenaline. The need for treatment depends on the haemodynamic consequences of the arrhythmia, which is not likely to be significant unless the rate drops below 40 beats per minute.
Bradycardia can occur just because someone is fit; many professional athletes will have a heart rate around 40 beats per minute. Bradycardia is also a major cause of blackouts, and can be very difficult to diagnose if it occurs rarely and is intermittent. Patients who black out will not always be aware of truly losing consciousness and may even "remember" tripping over. Occasionally even the occasional case of epilepsy can be cured with a pacemaker!
Dominic Cox, specialist registrar in cardiology, Newcastle upon Tyne
Hamish Dougall, general practitioner and research fellow in general practice, University of Dundee
studentBMJ 2001;09:443-486 December ISSN 0966-6494