Bradyarrhythmias: Types Causes Diagnosis Management by NJE


Bradyarrhythmias: bradycardia is defined as a heart rate <60 beats/min, and can be either physiological or pathological. Bradycardias are common in critically-ill patients and occur in about 10% of patients admitted to an intensive care unit (ICU). Here, a number of different factors may underlie the abnormal rhythm. As with any dysrhythmia, it is crucial to identify the abnormal rhythm correctly, to then allow prompt institution of appropriate management.

Types of Bradyarrhythmias

Bradyarrhythmias occur at three levels within the conduction system:

◆ Sino-atrial node.

◆ Atrioventricular node.

◆ Bundle branches.

Causes of Bradyarrhythmias

Patients in the critical care setting are often seriously ill with multisystem disorders and receive multiple therapies that can influence the conduction system. 

Types of cause of Bradyarrhythmias


Highly trained athletes have low resting heart rates (often in the range classified as bradycardia).


◆ General systemic:

•  Hypothermia.

•  Hypothyroidism.

•  Pain.

•  Vagal responses.

•  Raised intracranial pressure:  stroke, haemorrhage, encephalopathy.

•  Cholestatic jaundice.

•  Operations.

•  Sepsis.

•  Diabetes.

•  Intubation.

◆ Cardiovascular:

•  Degenerative conduction disease.

•  Ischaemic heart disease.

•  Valvular heart disease.

•  Cardiomyopathy.

•  Congenital heart disease.

•  Infiltrative disease.

•  Myocardial disease.

◆ Medications:

•  β-blockers.

•  Anti-arrhythmic drugs.

•  Digoxin.

•  Amiodarone.

•  Calcium antagonists.

•  Tricyclics.

•  Neuroleptics.

•  Dementia medications.

•  Toxins. 

Diagnosis of Bradyarrhythmias


Bradycardias are sometimes identified in asymptomatic patients who present for other reasons, but the arrhythmia may require management. Other patients present with dizziness, syncope, or seizures. In the critical care setting, a patient may present with a sudden drop in blood pressure, impairment of conscious level or hemodynamic collapse which, in some cases, may require immediate resuscitation. Many patients will be continually monitored and this will draw immediate attention to rate abnormalities.

Clinical examination

Palpating the pulse reveals bradycardia. Features of a low cardiac output state (peripheral shutdown, sluggish capillary refill) should always have bradycardia considered as an underlying cause.


The most critical diagnostic investigation is the electrocardiogram (ECG). The presence of the P wave and its relationship to the QRS complex are critically important features. ICU patients frequently have one- or three-lead monitoring as routine, although a formal 12-lead is preferable and may help elucidate the cause. In most cases, Holter and loop recorders are not required, since patients are already undergoing intensive monitoring.

Types of bradycardia

Sinus node disease

This is common and can affect any age group, but is particularly prevalent in the elderly. The sinus node receives rich innervations from the cardiac sympathetic and parasympathetic nerves and is therefore very sensitive to vagal influences and drugs.

Sinus bradycardia

Accounts for around 30% of all bradyarrhythmias and is manifested by a heart rate <60 beats/min which is inappropriate to the clinical state of the patient. The heart rate frequently fails to respond appropriately to exercise or activity.

Sinus bradycardia. Rate is below 60 beats/min, but each P wave is followed by a QRS complex.


P-wave slowing but each P wave is followed by a QRS complex.

Sinus arrest

This occurs when the SA node transiently fails to exhibit normal automaticity. The ECG demonstrates a pause without P waves and the length of the pause is not a multiple of the preceding P–P interval. Pauses of 2–3 seconds’ duration are seen in 11% of healthy asymptomatic individuals, whereas pauses >3 seconds during waking hours are usually due to sinus node dysfunction. These may lead to life-threatening asystole and therefore require treatment with either drug and/or pacing.

Sinus arrest. Sudden bradycardia is followed by an absence of P wave activity.
Sinus arrest—with infra-Hissian escape rhythm

Sinus exit block

The SA node fires, but the impulse is delayed or fails to propagate beyond the sinus node, resulting in failure of atrial depolarization. The ECG shows a pause without P waves. Type I second degree SA exit block demonstrates progressive P–P interval shortening before the pause (duration is less than two P–P cycles). In Type II second-degree sino-atrial exit block, the pause duration is theoretically an exact multiple of the previous P–P interval as the SA node continues to fire at its own intrinsic rate. Pauses with this condition are generally short and do not require treatment.


P-wave absence occurs with no QRS unless the patient has a junctional escape rhythm.

AV-nodal conduction disease

It is important to distinguish between block within the AV node and block within or below the His bundle (infranodal AV block), as both prognosis and appropriate treatment depend on this distinction. A surface ECG can assist in making this differentiation. Prolongation of the P–R interval before block (Wenckebach pattern) is strongly suggestive of AV nodal block, whereas sudden block without prolongation of the P–R interval is very suggestive of infranodal block. The escape rate in the setting of complete AV block is higher (40–60 beats/min) in AV nodal block, as the escape pacemaker is usually in the His/proximal Purkinje system. Infranodal block results in a less reliable, more distal (often ventricular) escape rhythm (heart rate <40 beats/min). The width of the QRS complex is also helpful: the QRS duration in AV nodal block is generally relatively narrow (<120 milliseconds), whereas the QRS duration in infranodal block is relatively wide.

1st-degree AV block

Commonly seen where each atrial impulse is successfully conducted to the ventricle but with a delay. This is of little importance as it does not affect cardiac physiology and generally does not require treatment. However, this is liable to progress to higher degrees of heart block and should alert the physician.

First-degree heart block. The PR interval is prolonged, but each P wave is followed by a QRS.


Each P wave is followed by a QRS, but with prolongation in the P–R interval >200 milliseconds.

When the QRS complex is narrow, the level of conduction delay is within the AV node in >90% of cases. First-degree AV block with a bundle branch block/wide QRS may represent infranodal conduction delay in up to 45% of patients.

Second-degree AV block–Mobitz type

In this condition, some atrial impulses fail to reach the ventricle. The surface ECG demonstrates some P waves that are not followed by a QRS complex.

Mobitz type 1 block. The PR interval demonstrates progressive prolongation until one fails to conduct.

Mobitz type 1 (Wenkebach block)

Most commonly associated with AV nodal conduction system disease (see Fig. 157.5). The P–R interval shows progressive prolongation with shortening of the R–R interval until a P wave fails to conduct to the ventricle, and then the cycle starts again. This type of block is usually not of importance and is unlikely to be harmful unless the degree of block progresses. Wenckebach block is almost always a result of block in the AV node, particularly when associated with a narrow QRS complex. The pause during this cycle is short. This block does not generally require pacing, but may herald of higher degrees of block.


PR-interval shows progressive prolongation until a P wave fails to conduct to the ventricle.

Mobitz type 2 block

The P wave fails to conduct to the ventricle and the previous QRS does not show any evidence of PR prolongation. The underlying QRS may be narrow or broad. This type of block can commonly occur nocturnally or in patients with high vagal tone, e.g. very fit individuals. Block during the day indicates more extensive conduction disease and usually merits pacing due to the unpredictable nature and duration of pauses. 

Mobitz type 2 block with 2-to-1 conduction from the atrium to the ventricle. The P wave is dropped without any PR prolongation on the previous complex.
The QRS is broad, suggesting infra-Hissian conduction system disease.


P wave fails to conduct to the ventricle and the previously conducted P-QRS does not show any evidence of PR prolongation.

3rd-degree (complete) heart block

Here, the atria and ventricles function independently. The P wave has no relation to the QRS, which can be narrow or broad, and the level of block can be either in the AV node or infranodal. Acquired causes (which predominate in the ICU care setting) are often infranodal and potentially life-threatening. A  common exception is after acute inferior myocardial infarction where the block is generally nodal and frequently reversible. Digitalis toxicity is a common cause of reversible AV block.

      Prognostically, patients with a narrow QRS fare better than those with more extensive disease who demonstrate broad QRS com￾plexes. Although some patients with complete heart block and narrow QRS can be left unpaced (e.g. congenital complete heart block), those with a broad QRS nearly always need pacing.

Complete heart block with an infra-Hissian escape rhythm. The P waves have no relationship to the QRS complexes


The P wave has no relationship with the QRS.

Infra-Hisian conduction block

Right-bundle branch block

This can commonly be found in individuals where the heart is structurally normal. This usually does not need intervention.

Left bundle branch blocks

Left anterior fascicular block, left posterior fascicular block, and complete left bundle branch block are much more likely to be associated with underlying cardiac disease, are frequently progressive, and may require pacemaker insertion.

  These blocks are important when associated with sinus and AV nodal abnormalities since they suggest more extensive disease of the conduction system that may fail suddenly.

Management of Bradyarrhythmias

Identification of the type of bradycardia is of critical importance to management. Particular interventions are likely to precipitate bradycardia in the critical care setting [5]. These include intubation, endotracheal suction, and sometimes bladder catheterization. In patients who demonstrate this tendency, the prior administration of glycopyrroniumbromide (0.1 mg IV) or 600 µg atropine before the intervention may avoid the bradycardia. Rarely patients may have several seconds of asystole in association with the intervention and this is not responsive to anticholinergics. In these cases insertion of a temporary pacing electrode prior to the intervention may be required.

In the acute setting where the patient suddenly becomes bradycardic or asystolic acute resuscitation may be required. A precordial thump may occasionally reverse asystole and start the heart beating again. If this does not occur, cardiorespiratory resuscitation may be required and should be maintained until pacing can be initiated.

Pacing should also be initiated in patients who do not respond to atropine (or second-line drugs). Pacing is also recommended for severely symptomatic patients, especially when the block is at or below the His-Purkinje level (i.e. type II second-degree or third-degree AV block).



The first-line drug for acute symptomatic bradycardia with an initial dose of 0.5 mg intravenous (iv) every 3–5 minutes to a maximum total dose of 3 mg. Atropine reverses cholinergic-mediated decreases in heart rate, symptomatic sinus bradycardia, symptomatic high-degree AV block and any type of AV block at the nodal level. The increased heart rate caused by atropine in acute coronary ischemia or myocardial infarction may worsen the ischemia or increase the zone of infarction so this drug must be used cautiously. Avoid relying on atropine in type II second-degree or third-degree AV block or in patients with third-degree AV block with a new wide-QRS complex. These patients require immediate pacing.

Alternative drugs

May be considered with bradycardias that are unresponsive to atropine, while awaiting the availability of a pacemaker:

◆ Adrenaline:  infusion at 2–10  μg/min and titrate to patient response. Provide intravascular volume and support as needed.

◆ Dopamine: infusion (at rates of 2–10 μg/kg/min) can be added to epinephrine, or administered alone.

◆ Isoprenaline: infuse at 2–10 µg/min and titrate against heart rate response. This drug is more likely to raise the blood pressure, but patients can often be maintained for several hours before pacing is initiated.

◆ Glucagon:  one case series documented improvement in heart rates with iv glucagon (3 mg initially, followed by infusion at 3 mg/hour if necessary) when given to patients with drug-induced bradycardia not responding to atropine.


Several modalities of pacing are available including external, oesophageal, and transvenous.

External pacing

Transcutaneous external pacemakers have a special pulse duration, surface electrodes, and a current generator:

◆ Pulse duration: long electrical pulse duration are used (40 milliseconds pulses for Zoll or 20 milliseconds pulses for all others).

◆ Electrodes: large surface electrodes (80–100 cm2) are used since pain is directly related to the amount of current delivered and inversely related to the skin surface area over which it is delivered. Thus, pain is minimized by using electrodes with large surface areas.

◆ Current: the average current necessary for external pacing ranges from 50 to 100 milliamperes (mA). This delivers approximately 0.1 Joules (J), below the 1–2 J required to cause an uncomfortable tingling sensation in the skin. Transcutaneous external pacemaker discomfort at these low levels of current delivery is due to the force of skeletal muscle contraction, rather than the electric current. More than 90% of patients tolerate pacing for ≥15 minutes with modern devices capable of delivering up to 140–200 mA.

◆ Before beginning transcutaneous external pacing, the patient should be informed of the reason for pacing, the discomfort that may be experienced, and the option of providing analgesia or sedation, if possible.

◆ Pad application: pacemaker pads are applied over the cardiac apex and just medial to the left scapula. Excessive body hair should be shaved to ensure good contact.

◆ Pacemaker operation: heart rate should be set to 80 beats/min and the current initially set to 0 milliamperes (mA). The pacemaker unit is turned on, and the current increased in 10 mA increments until capture is achieved. Capture should be confirmed by palpable carotid pulses, and ECG evidence on monitoring.

◆ Synchronous/asynchronous modes:  in the asynchronous (fixed-rate) mode, the electrical stimulus is delivered at preset intervals, independent of intrinsic cardiac activity. Synchronous pacing is a demand mode in which the pacer fires only when no complex is sensed for a predetermined amount of time. Generally, pacing should be started in synchronous mode.

◆ Minimizing discomfort:  sedation with a short-acting agent, such as midazolam or an opiate, should be considered.

◆ Complications: pain, coughing, and hiccoughs may result from stimulation of the diaphragm and thoracic muscles. Skin burns have been reported with prolonged use.

Oesophageal pacing

A specialized pacing electrode can be placed via the esophagus and manipulated to 30–40 cm from the teeth. At this level, the left atrium is in close proximity and pacing can give atrial capture reliably using a special stimulator, which has long amplitude pulses with high amplitude. Ventricular stimulation is less reliable because of the greater distance of the esophagus from the ventricle; this technique should not be used for atrioventricular block. Leads inserted via the nostril (similar to nasogastric tubes) can be maintained for several days. Complications include oesophageal discomfort (rarely, burns with high outputs) and phrenic nerve stimulation.

Temporary intracardiac pacing

A pacing electrode is inserted through an introducer sheath sited in the subclavian or internal jugular vein (rarely, femoral) and then fluoroscopically guided to the right ventricular apex. In an emergency situation, a flotation electrode can be used. This is a Swan–Ganz type of balloon catheter with pacing electrodes. It is floated from the entry site into the heart with the electrocardiogram being recorded. When a ventricular trace is obtained, the pacing is commenced, the balloon deflated and the lead secured. Pacing thresholds of <1 mV with a pulse duration of 0.5 milliseconds are satisfactory. Leads can also be placed in the atrium; specialized leads with screw-in tips are available designed for atrial pacing. Placement of leads in the atrium and ventricle allows co-ordinated atrioventricular pacing. These leads do not cause discomfort and pacing can be maintained for several days.

Complications are generally related to access (pneumothorax, hematoma, air embolism), myocardial perforation leading to tamponade, ventricular arrhythmias, and infection.

Permanent pacemaker insertion

A permanent pacing system can be acutely implanted for the treatment of sudden onset bradycardia without a reversible cause and at the discretion of the managing physician.



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