Cardiac rhythm interpretation is one of the most important skills EMS providers must master. It’s essential to be able to rapidly and accurately interpret rhythm disturbances, as patients with tachy- and brady-dysrhythmias may be unstable and require emergent assessment and treatment. While an in-depth review of all such arrhythmias is outside the scope of this article, we will focus on the diagnosis and treatment of a subset of bradydysrhythmias, specifically AV block and conduction delay.
Before discussing the abnormal electrical conduction in the heart, it’s important to first understand the anatomy of the cardiac conduction system and normal conduction patterns.
The heart is composed of three specialized cells: 1) pacemaker cells; 2) Purkinje cells; and 3) contractile cells.1 Pacemaker cells have a property called automaticity; they undergo spontaneous electrical depolarization that initiates an electrical impulse. The Purkinje cells conduct electrical impulses more quickly than other cells, so that electrical impulses are easily conducted through them. Contractile cells compose the large majority of the heart and will contract when the electric depolarization reaches them.
Typically, electrical impulses in the heart begin in the sinoatrial (SA) node, which is located in the right atrium and contains pacemaker cells. The sinus node artery supplies the SA node; it arises from the right coronary artery (RCA) about 55% of the time and the left circumflex artery (LCx) about 45% of the time.1 From the SA node, impulses then travel through the atrial myocardium to the atrioventricular (AV) node, which lies at the junction between the atria and the ventricles.2
A fibrous ring called the annulus fibrosis electrically insulates the atria and ventricles from one another; thus, the only way for electrical impulses to travel between the atria and ventricles is through the AV node.
The blood supply to the AV node is from the RCA in 90% of people and from the LCx in 10%.1 The distal continuation of the AV node is the bundle of His (sometimes referred to as the atrioventricular bundle), which is composed of Purkinje cells and travels down the intraventricular septum.1–3
The bundle of His separates into two distinct bundles a few millimeters below its junction with the AV node: the left and right bundle branches. The bundle of His is connected to the AV node, but is electrically insulated from the surrounding myocardium, thus allowing conduction only down the bundles rather than directly into the surrounding cardiac tissue. The bundle of His separates into the right and left bundle branches; the left bundle branch further subdivides into an anterior and posterior component.2
“Heart block” refers to a variety of conditions in which conduction from the atria to the ventricles is delayed. We will review the differing types of AV block along with associated causes and treatment.
First-degree AV block is due to delayed conduction in the atrium, AV node or in the His-Purkinje system.4,5 On an ECG, this manifests as a prolonged PR interval with a duration greater than 20 ms. Though the PR interval is prolonged, it should remain constant, and a P wave should precede every QRS complex. Most cases of first-degree AV block will also have a narrow QRS complex, indicating the block is in the proximal portion of the conducting system—likely the AV node itself;4,6 approximately 13% of first-degree AV block, though, may have a wide QRS, indicating a more distal block.4
Approximately 1–2% of the population may have a first-degree AV block as a normal variant; it has no relation to ischemic heart disease and no prognostic value. Clinically, these patients usually have a benign presentation.4 Most patients are asymptomatic and the AV block is found incidentally.4,7 Patients may rarely present with symptoms such as palpitations, dizziness, syncope or angina. Most of these symptoms are due to low cardiac output secondary to the AV block. First-degree AV block can also rarely be seen as a manifestation of acute rheumatic fever or more commonly from medication side effects.4
In an asymptomatic patient, no further investigation or treatment is recommended, though some recent literature has shown that patients with first-degree AV block have an increased risk of developing atrial fibrillation.4,7
Second Degree Type I
Second-degree type I AV block is also known as Mobitz type I or Wenkebach.4 Mobitz type I block is classically characterized by a progressive lengthening of the PR interval culminating in a dropped QRS complex. The site of the block is usually at or above the AV node, so the P wave and QRS complex will generally have a normal morphology and duration.4,6 As the PR interval lengthens, the R-R interval shortens on the rhythm strip.6 In the first beat of the series, the PR interval will be of normal duration; subsequent beats will have a progressively longer PR interval until the P wave is unable to reach the ventricles and cause a depolarization. This results in a dropped beat, after which the cycle begins again.4
The conduction disturbance in Mobitz type I block is in the AV node approximately 72% of the time, as opposed to within or below the bundle of His. Generally, these may be distinguished by the width of the QRS complex: A complex with normal duration indicates a block in the AV node whereas a widened QRS indicates a block either within or below the bundle of His.4 A simple way to remember this is that if conduction is delayed above the bundle of His, once it passes the block the impulse will still be conducted normally, so the QRS complex should appear normal.
Mobitz type I blocks can sometimes be seen in normal people while asleep and also in conditioned athletes, though both of these are rare findings. It can also be associated with acute myocardial infarction (MI) and as a result of antiarrhythmic or rate-controlling medications. Similar to a first-degree AV block, many patients will be asymptomatic at presentation.
Prognosis and treatment of Mobitz type I depends on symptoms and presence of underlying heart disease. Patients who are asymptomatic and have no heart disease generally don’t require treatment. Asymptomatic patients with underlying heart disease have a variable prognosis, but the prognosis is related to the progression of the underlying heart disease as opposed to the AV block itself. Progression to a higher grade of AV block is rare, unless the patient is experiencing an acute MI. In some patients, a Mobitz type I block will cause symptoms of hypoperfusion, such as dizziness, syncope or hypotension.
EMS providers who encounter symptomatic patients with Mobitz type I heart block should treat the patient with atropine to increase heart rate and therefore perfusion.4 Atropine should be given as a bolus dose of 0.5 mg, and the standard recommendation is to repeat a dose of 0.5 mg every three to five minutes as needed, with the total dose to not exceed 3 mg.4,7 If the first dose of 0.5 mg of atropine is ineffective, our recommendation is to increase the second dose to 1.0 mg one to two minutes after the initial dose is given. We feel waiting three to five minutes to give another 0.5 mg in a symptomatic patient isn’t aggressive enough in the prehospital setting. If atropine is ineffective and the patient remains symptomatic, temporary pacing may be indicated. As Mobitz type I block is generally benign, pacing is only indicated if the patient is hemodynamically unstable or has syncope, symptoms of acute congestive heart failure or ischemic chest pain.
Second Degree Type II
Second-degree type II AV block is also known as Mobitz type II.4 It’s also characterized by non-conducted P waves, or dropped QRS complexes. The PR interval in Mobitz type II may be normal or prolonged, but unlike Mobitz type I, it remains constant.4,6 The dropped beats will generally, but not always, occur at regular intervals.7 The QRS complex may be narrow but is more often widened, due to associated bundle branch blocks or the infranodal location of the block. The location of the block in Mobitz type II is distal to the bundle of His, either in the common bundle or the bundle branches. The block can be expressed as a ratio of P waves to QRS complexes; for example, three P waves to every two QRS complexes would be a 3:2 block.4,6
EMS providers must quickly recognize second-degree type II AV block as it’s a much more ominous rhythm than second-degree type I. Patients with Mobitz type II blocks may be unstable, and can suddenly progress to a third-degree heart block, so vigilance is warranted at all times.4,7 Patients with large anterior wall infarctions are at particular risk of progression to complete heart block. As with any bradycardia, the need for emergent treatment is dictated by patient stability.
Patients who are unstable at the time of assessment or progress to complete heart block will require immediate treatment. Although atropine can be tried early on, it’s generally unhelpful, as its predominant effect is to increase the sinus node’s rate and is less effective in increasing AV conduction.
Paramedics shouldn’t waste significant time with atropine if the initial dosing doesn’t improve the patient’s heart rate, as these patients usually require transcutaneous pacing. At the hospital, even asymptomatic patients are likely to undergo permanent pacemaker placement due to the risk of deterioration into complete heart block.4
Distinguishing between Mobitz type I and type II blocks is particularly difficult in patients who have a 2:1 AV block where every other beat is dropped.4,6 Unless a care provider is able to capture two consecutively conducted impulses, distinguishing between the two is impossible, and the rhythm can be referred to as a second-degree AV block with a 2:1 conduction pattern, or nontypeable AV block.4 A trick that can be used is to use the width of the QRS complex as a clue, as a wide QRS complex is more common in Mobitz type II and narrow QRS complex is more common in Mobitz type I.6 Symptomatic patients with a nontypeable second-degree AV block warrant a trial of atropine, particularly when the QRS is narrow, as this indicates a block above the bundle of His. Patients who have a stable, wide QRS 2:1 block or a block that evolves into a type II block aren’t likely to respond to atropine; rapidly switching to pacing is recommended for these patients.4
Second-degree AV block is considered high-grade or advanced when two or more consecutive P waves are blocked.4,6 In patients with an anterior MI, this is usually due to a second-degree type II AV block with co-existent bilateral bundle branch blocks.4 These patients are at particularly high risk for progression to complete heart block.6
Third-degree, or complete AV block, is characterized by a complete dissociation between the atria and ventricles due to absence of conduction through the AV node.4,5 Since no atrial impulses reach the ventricles, the ventricular rate is determined by either a junctional or ventricular pacemaker, which is inherently slow.4 Both the P waves and QRS complexes will “march out” regularly on the ECG, yet be unrelated.6,7
Since the P wave is not generating a QRS complex they may be buried in the complex itself, or in the T wave. If there’s a junctional pacemaker, the QRS complex will be narrow with a rate of 40–60; a ventricular pacemaker will produce a wide QRS complex with a rate of 20–40. These rhythms are generally referred to as either junctional or ventricular “escape” rhythms.4 Ventricular escape rhythms are more likely to be acquired and generally associated with a poorer prognosis.6 The atrial pacemaker may be the SA node or an ectopic focus; thus, the atrial rate may be normal, bradycardic, tachycardic, flutter or fibrillation, while the ventricular rate will generally be bradycardic but regular.4,6 The atrial rate will generally be higher than the ventricular rate, although occasionally the two are very similar; in these cases the block is referred to as “isorhythmic.”4
There are many causes of complete heart block such as ischemia, electrolyte disturbances, tumors, cardiomyopathy, myocarditis, hypothyroidism and hypothermia. The incidence increases with advancing age.5 In adults, the most common causes are drug toxicity (generally from rate-controlling medications), coronary artery disease and degenerative processes.4 In children, the most common cause of complete AV block is congenital: abnormal development of the AV node.4
Third-degree heart block can occur in the setting of acute MI, and these patients are at high risk of hemodynamic instability.4,5 Symptoms are due to decreased cardiac output and may include dizziness, syncope, angina and sudden cardiac death. Elderly patients may only complain of weakness or fatigue. Patients with anterior MI are more likely to be unstable initially, or to suddenly develop instability, because anterior ischemia from occlusion of the left anterior descending artery will cause ischemia and delayed conduction of the bundle branches and conduction system distal to the bundle of His.4,5 In such patients, it’s prudent to place pacing pads at the initial encounter and prior to transport, in case of sudden need for transcutaneous pacing. If a transcutaneous pacemaker isn’t immediately available in the symptomatic patient, a trial of atropine is warranted, though unlikely to increase cardiac output.4
Use of Atropine
Atropine is a parasympatholytic agent; it has vagolytic action that predominantly increases the sinus node’s rate, thus it’s especially effective in sinus bradycardia. This decrease in vagal tone may sometimes also increase AV conduction. Along with this, it also acts on the more distal components of the conduction system. The goal when using atropine is to increase cardiac output and therefore systemic perfusion. It’s most effective in patients with acute myocardial ischemia or infarction, as opposed to patients with primary conduction system disease, as acute MI patients have heightened parasympathetic tone.8,9 As mentioned previously, studies have shown that atropine is more effective in patients with sinus bradycardia than AV block, and more effective with AV block occurring early in the course of acute MI.8
Prehospital administration of atropine has been shown to be safe and effective in bradycardia due both to acute MI and non-acute MI. Complications from atropine administration are rare and include ventricular fibrillation, ventricular tachycardia and symptomatic PVCs. Additionally, there’s thought that during an acute MI, atropine may worsen ischemia by increasing heart rate and therefore metabolic demand of the heart, though one must keep in mind that ischemia is also worsened by hypoperfusion due to the bradyarrhythmia itself. As with any drug, careful selection of patients and awareness of potential adverse effects of atropine are paramount for all providers.8 With any patient who’s symptomatic enough to require pharmacotherapy, always also plan for initiation of transcutaneous pacing in the event that the medication isn’t effective.7
In circumstances where atropine is not effective, providers must be prepared to initiate transcutaneous pacing. The purpose of cardiac pacing is to deliver an electrical current to the heart to stimulate contraction of the myocardium.10 Both pacing-only electrodes and multifunction electrodes are available; multifunction pads are capable of pacing, monitoring and defibrillation, and are more commonly found in the prehospital setting. It’s important to be familiar with the equipment available to you.
There are two options for pad application to the patient. The anterior-posterior configuration is preferred: The anterior pad is placed over the left anterior chest at the position of lead V3, and the posterior pad is placed on the back between the left scapula and the thoracic spine. Alternatively, the first pad is placed on the right upper chest and the second pad placed on the left side of the chest near the apex of the heart.7,10 This positioning may be preferable when the patient develops the need for pacing during transport or when access to the patient’s back may not be possible.
Once the pacemaker pads are applied to the patient, two variables must be adjusted on the machine: rate and output. Pacemakers operate on either a fixed-rate or demand mode. Fixed-rate pacing produces an electrical impulse at the set rate no matter the intrinsic cardiac activity of the heart, while demand pacing will only deliver an electrical impulse if the patient’s heart rate falls below the set rate. Fixed-rate pacing is used in the prehospital setting, and one should generally set a rate of between 60–90, depending on local protocols.10 The electrical output should begin on the lowest setting, and the provider should observe a pacing spike on the monitor. The current should then be increased by five to 10 mA at a time until a QRS complex and T wave appear after each pacer spike. This is termed “electrical capture.”
Once electrical capture has been achieved, one should next feel for a pulse to ensure mechanical capture. For transcutaneous pacing to be successful, you must have both electrical and mechanical capture. Once mechanical capture is achieved, the electrical output is turned down until mechanical capture is lost; this is the pacing threshold, and will generally be between 40 and 80 mA. The current should be increased five to 10 mA above the pacing threshold in order to ensure continued mechanical capture with the least amount of energy required.7,10
The pacing threshold often increases over time, so continually observe the patient and check pulses frequently; increase the current as needed to ensure mechanical capture.10 Keep in mind transcutaneous pacing can be quite painful, so consider providing pain management and sedation as appropriate. It’s not uncommon for transcutaneous pacing to be ineffective in increasing heart rate and thus cardiac output. In such cases, providers may need to move to more aggressive pharmacotherapy, such as a continuous epinephrine infusion, as guided by protocol.
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2. Kawashima T, Sasaki H. Gross anatomy of the human cardiac conduction system with comparative morphological and developmental implications for human application. Ann Anat. 2011;193(1):1–12.
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4. Hayden GE, Brady WJ, Pollack M, et al. Electrocardiographic manifestations: Diagnosis of atrioventricular block in the emergency department. J Emerg Med. 2004;26(1):95–106.
5. Barra SN, Providência R, Paiva L, et al. A review on advanced atrioventricular block in young or middle aged adults. Pacing Clin Electrophysiol. 2012;35(11):1395–1405.
6. Ufberg JW, Clark JS. Bradydysrhythmias and atrioventricular conduction blocks. Emerg Med Clin N Am. 2006;24(1):1–9.
7. Deal N. Evaluation and management of bradydysrhythmias in the emergency department. Emerg Med Pract. 2013;15(9):1–15.
8. Swart G, Brady WJ, DeBehnke DJ, et al. Acute myocardial infarction complicated by hemodynamically unstable bradyarrhythmia: Prehospital and ED treatment with atropine. Am J Emerg Med. 1999;17(7):647–652.
9. Brady WJ, Swart G, DeBehnke DJ, et al. The efficacy of atropine in the treatment of hemodynamically unstable bradycardia and atrioventricular block: Prehospital and emergency department considerations. Resuscitation. 1999;41(1):47–55.
10. Gibson T. A practical guide to external cardiac pacing. Nurs Stand. 2008;22(20):45–48.
>> Understand the physiology and anatomy of the cardiac conduction system and normal conduction patterns.
>> Identify the different degrees and types of AV block through accurate interpretation of rhythm disturbances.
>> Learn how to treat AV block patients, including the administration of atropine and transcutaneous pacing.