Patients admitted with bradycardia may present with a variety of clinical pictures, ranging from fatigue to syncope and cardiac arrest. It is important to be able to identify the mechanism of bradycardia in order to distinguish benign from life-threatening situations.
In general, sinus bradycardia or arrest, as well as atrioventricular block (AVB) at the nodal level, have a benign prognosis. Infranodal block (bundle of His or bundle branches) may lead to prolonged asystole without an escape rhythm. Proper clinical evaluation will lead to appropriate therapeutic measures, whereas mismanagement may have a fatal outcome.
Obviously, not all documented bradycardia needs treatment and, conversely, undocumented but suspected bradycardia may need backup measures to avoid asystole. Overall, therapy for bradycardia aims to (1) avoid asystole, (2) improve haemodynamic status, or (3) avoid tachycardia (e.g., in the setting of a prolonged QT interval with torsades de pointes). Management strategies for bradycardia depend upon a number of factors, listed below:
– Presence, duration and gravity of symptoms (for how long has the patient been symptomatic? Was there syncope? If yes, did it result in trauma?)
– Vital signs
– Systemic repercussions of bradycardia and a low-output state (renal function, lactate, etc.)
– Type of bradycardia (sinus, AVB II Wenckebach vs Mobitz 2, AVB III)
– Presence or absence of a documented escape rhythm
– Effect of pharmacological treatment (isoprenaline, atropine)
– Anticipated duration of the bradycardia
Nodal AVB can be distinguished from infranodal AVB by careful analysis of the electrocardiogram and by diagnostic bedside manoeuvres (table 1). AVB III may occur at both nodal as well as infranodal levels, although the latter is more frequent. High-grade AVB is defined as ≥3:1 AVB. A common mistake is to misdiagnose AVB III by failing to recognise conducted P waves (fig. 1).
|Table 1: Clues to help distinguish nodal from infranodal atrioventricular block.|
|Nodal block||Infranodal block|
|Diagnostic / strongly suggestive||AVB II Wenckebach (may exceptionally be infranodal!)||AVB II Mobitz 2|
|Long PR when conducting||Normal PR when conducting|
|PP prolongation before AVB||No PP prolongation|
|During sleep only||Occurs at exercise (e.g. isometric bedside manœuvres)|
|Provoked by CSM||Worsened conduction with atropine/catecholamines|
|Improved conduction with Atropine/catecholamines||Improved conduction with CSM|
|Suggestive||Narrow QRS (however, intra-Hissian block may result in a narrow QRS!)||Wide QRS (however the patient may have nodal block with concomittent bundle branch block!)|
2:1 or 3:1 AVB
|BB, diltiazem, verapamil, digoxin||Flecainide, propafenone|
|AVB = atrioventricular block; BB = beta-blockers; CSM = carotid sinus massage|
In 2015, the European Resuscitation Council published guidelines on advanced life support , which include an algorithm for the acute management of bradycardia (fig. 2).
Pharmacological therapy is most often the first line of treatment for bradycardia because it is the most readily available. A list of the drugs used is shown in table 2. It should be noted that drugs that increase sinus rate may worsen infranodal block. However, in the case of infranodal AVB III, heart rate may increase with infusion of catecholamines (e.g., isoprenaline) owing to acceleration of the automatic escape rhythm, and may therefore be of therapeutic interest despite lack of improvement in AV conduction. Pharmacological treatment for bradycardia due to drug toxicity is summarised in table 3.
|Table 2: Drugs used to increase heart rate.|
|Atropine||Muscarinic acetylcholine receptor antagonist||0.5 mg i.v. (repeat every 3–5 minutes to max. 3 mg)||t½ 3−4hours. ~50% renal excretion.||Indicated in case of nodal block. Doses <0.5 mg may paradoxically worsen bradycardia. CI: glaucoma, prostatism, illeus|
isoproterenol||Alpha-1, alpha-2, beta-1 and beta-2 adrenoreceptor agonist||Start infusion at 4 μg/min then up-/down-titrate over minutes to 1−10 μg/min based upon response||t½ 1 min||May not be well tolerated over many hours because of side effects (trembling, headache, etc)|
|Adrenaline/ epinephrine||Alpha and beta adrenoreceptor agonist||Infusion 2–10 μg/min (titrate with response)||t½ 3 min followed by slower elimination (t½ 10 min)||Useful if hypotension is an issue (owing to vasoconstricting effect)|
|Dopamine||Dopamine and alpha and beta adrenoreceptor agonist||Infusion 4−10 μg/kg/min||t½ 2 min||No bolus injections|
|Dobutamine||Beta-1 adrenoreceptor agonist||Infusion 3−10 μg/kg/min||t½ 2 min||Useful if concurrent inotropic insufficiency|
|Theophylline||Adenosine receptor antagonist and phosphodiesterase inhibitor||100−200 mg slow i.v. injection||t½ 4−24 h (affected by age, smoking, hepatic function, drug interactions, etc.)||Infrequently used for treating bradycardia|
|Aminophylline||Adenosine receptor antagonist and phosphodiesterase inhibitor||200−300 mg slow i.v. injection||Infrequently used for treating bradycardia|
|All drugs should be used with caution in cases with cardiac ischaemia. t½ = half-life; CI = contraindication|
|Table 3: Specific treatment options for bradycardia due to drug toxicity.|
|Drug causing bradycardia||Treatment||Comments|
2–10 mg bolus followed by 2–5 mg/h infusion
|Inotropes: adrenaline, dobutamine, isoprenaline||Competitive beta-receptor agonists|
High doses often required to overcome the effect of beta-blockade
|Calcium channel blocker||Intravenous calcium||First-line antidote|
Partially overcomes calcium blockade
Calcium chloride or calcium gluconate can be given as boluses or infusion—monitor levels
|Glucagon||Can be used as bolus or infusion: 2–10 mg bolus followed by 2–5 mg/h infusion|
|Digoxin||Digoxin-specific antibodies (Fab fragments)||First-line antidote Allergenic and expensive. Only to be used in life-threatening arrhythmias attributed to digoxin.|
This modality is readily available, usually effective (if properly delivered), but underused in clinical practice because of reluctance to cause discomfort to the patient. It is suitable as an emergency life-saving measure, or as a backup for infrequent pacing (e.g., paroxysmal AV block, transient sinus asystole following cardioversion of atrial fibrillation, etc.). It is delivered using external defibrillators, but not all models offer this option. Pacing output can usually be set between 20–180 mA. It is important to place the patches in an anteroposterior position (fig. 3), ideally over bony surfaces (pain being caused by skeletal muscle contraction). The pads should not be repositioned, as they may lose conductive gel and adhere less well.
In a conscious patient, the initial output may be set at, for example, 80 mA. In an unconscious patient, output may be programmed to the maximal value, and then down-titrated as appropriate. In a pre-hospital setting in 32 patients, average capture thresholds were 64 ± 33 mA .
Presence of ventricular capture should be verified by evaluating the patient’s pulse either manually or using an oximeter (fig. 4), as the ECG may be deceptive or difficult to analyse (figs 4 and 5). Obviously, pectoral muscle contraction does not indicate myocardial capture!
It is important to verify adequate sensing by checking that sensing markers are properly aligned with each intrinsic QRS complex (fig. 6).
In the event of undersensing, unnecessary pacing may be delivered (which may be potentially pro-arrhythmic if it falls on a T wave).
In the case of oversensing (e.g., of artefacts), pacing may not be delivered (even in the case of asystole). As sensitivity levels usually cannot be modified, a different lead vector needs to be chosen if there are sensing issues. As the external defibrillator may rely on cable electrodes for sensing, these should be properly fastened (if necessary secured by tape).
The backup pacing rate is usually set to a low value (e.g., 30 bpm) to avoid unnecessary pacing, and should be set with an output that is likely to result in capture e.g., 160 mA).
If transcutaneous pacing is expected to be ineffective (e.g., in an obese patient), it is wise to test capture first (see fig. 5). If necessary, patients may be sedated with analgesia.
This modality has been abandoned at our institution. A pacing wire is inserted into the oesophagus via the nose in order to pace the left atrium (which lies just anteriorly).
This modality is therefore not suitable for pacing in cases of AV block, and also provides inconsistent capture.
Temporary transvenous pacing doubles the risk of subsequent permanent pacemaker infection , and is associated with a risk of serious complications such as perforation and tamponade.
According to the 2013 European Society of Cardiology (ESC) guidelines on pacing , temporary transvenous pacing should be used “only as a last resort when chronotropic drugs (e.g., isoproterenol, epinephrine, etc) are insufficient” and “should be limited to cases of (i) high-degree AV block without escape rhythm, (ii) life-threatening bradyarrhythmias, such as those that occur during interventional procedures (e.g., during percutaneous coronary intervention, etc) or, rarely, in acute settings such as acute myocardial infarction, drug toxicity or concomitant systemic infection.”
The 2015 ESC guidelines on prevention of sudden death are equally restrictive on use of temporary transvenous pacing .
Venous access is most often obtained via the femoral vein, although it is also possible to place pacing wires via the internal jugular or subclavian vein (the latter may, however, compromise future permanent pacemaker implantation because of sterility or thrombotic issues). Pacing from the femoral vein requires the patient to stay lying and relatively immobile, as there is a risk of lead dislodgment. It is therefore unsuitable for agitated patients.
Temporary pacing wires are sized from 4–6 F. Thinner wires are less traumatic but less stable, whereas thicker wires carry a higher risk of perforation (fig. 7). Some wires have inflatable balloons just behind the tip designed to facilitate placement of the wires in the right ventricle (e.g., if fluoroscopy is not available). The balloon, if left inflated, may protect the patient from perforation by the lead (but stability needs to be verified under fluoroscopy). Temporary pacing of the atrium, although feasible, is rarely used because stability is a major issue.
There are sparse data in the literature on complications associated with temporary pacing. Dislodgment is a frequent issue, therefore sensing and capture thresholds need to be checked periodically (at least daily), with continuous rhythm monitoring. Perforation and tamponade may occur at any time after placement, and sometimes become manifest only after the temporary lead is withdrawn. Another issue is inadvertent placement of the lead via a patent foramen ovale into the left ventricle, with the risk of stroke (see fig. 7).
When temporary pacing is required for more than a few days or in the atrium, a standard pacemaker screw-in lead may be implanted via the internal jugular vein and connected to a recycled pacemaker (fig. 8). This allows pacing for up to 6 weeks  or more, allows mobilisation (and in selected cases even temporary discharge) of the patient, provides reliable pacing and sensing, and has a lesser risk of perforation than with temporary wires (which are stiffer).
Bradycardia is a frequently encountered issue in the emergency setting, and is a potential cause of mortality if inappropriately managed. Identification of high risk patients requires careful clinical evaluation and electrocardiographic analysis. Importantly, localisation of the site of AV block through ECG analysis and provocative manoeuvres allows delivery of appropriate therapy. Therapeutic strategies for persistent or suspected bradycardia in the emergency setting include pharmacological measures as well as temporary pacing, either transcutaneous or transvenous. Emergency medical teams should be well trained in the delivery of these therapies, as they may be life saving.
1 Soar J, Nolan JP, Bottiger BW, Perkins GD, Lott C, Carli P, et al. European Resuscitation Council Guidelines for Resuscitation 2015: Section 3. Adult advanced life support. Resuscitation. 2015;95:100–47.
2 Morrison LJ, Long J, Vermeulen M, Schwartz B, Sawadsky B, Frank J, et al. A randomized controlled feasibility trial comparing safety and effectiveness of prehospital pacing versus conventional treatment: ‘PrePACE’. Resuscitation. 2008;76:341–9.
3 Polyzos KA, Konstantelias AA, Falagas ME. Risk factors for cardiac implantable electronic device infection: a systematic review and meta-analysis. Europace. 2015;17:767–77.
4 Brignole M, Auricchio A, Baron-Esquivias G, Bordachar P, Boriani G, Breithardt OA, et al. 2013 ESC guidelines on cardiac pacing and cardiac resynchronization therapy: the task force on cardiac pacing and resynchronization therapy of the European Society of Cardiology (ESC). Developed in collaboration with the European Heart Rhythm Association (EHRA). Europace. 2013;15:1070–118.
5 Priori SG, Blomstrom-Lundqvist C, Mazzanti A, Blom N, Borggrefe M, Camm J, et al. 2015 ESC Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: The Task Force for the Management of Patients with Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death of the European Society of Cardiology (ESC). Endorsed by: Association for European Paediatric and Congenital Cardiology (AEPC). Eur Heart J. 2015;36:2793–867.
6 Kawata H, Pretorius V, Phan H, Mulpuru S, Gadiyaram V, Patel J, et al. Utility and safety of temporary pacing using active fixation leads and externalized re-usable permanent pacemakers after lead extraction. Europace. 2013;15:1287–91.
a University Hospital of Geneva, Switzerland; b Nyon regional hospital, Switzerland
No financial support and no other potential conflict of interest relevant to this article was reported.
Haran Burri, MD
University Hospital of Geneva (HUG)
Rue Gabrielle Perret-Gentil 4
CH-1205 Genève 14
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