The following medications can affect different levels of conduction delay: 

1) Increased parasympathetic tone, digoxin (which upgrades vagotonic action), calcium channel blockers (which obstructs the inward calcium current responsible for depolarization) and beta-blockers can affect the AV node 

2) Medications such as procainamide, quinidine, and disopyramide can block sodium channels and delay conduction in the bundle of His

3) Similarly though rarely, medications such as procainamide, quinidine, and disopyramide can also delay infra-Hisian conduction system 

History taking for patients with concerns for AV block should include: 

• History of heart disease, both congenital and acquired
• Full list of medications and dosing. Particular drugs of interest include beta-blockers, calcium channel blockers, antiarrhythmic drugs, digoxin
• Recent cardiac procedure 
• Signs and symptoms associated with other systemic diseases associated with heart block (amyloidosis, sarcoidosis) 
• Baseline exercise capacity 
• Potential expose to tick bites

 The following symptoms should raise concerns: 

• Dyspnea
• Fatigue
• Chest pain
• Presyncope or syncope
• Sudden cardiac arrest 

First degree. In first-degree AV block, the P waves always precede the QRS complexes, but there is a prolongation of the PR interval. That is, the PR interval will be greater than 200 milliseconds in duration without any dropped beats. There is a delay, without interruption, in conduction from the atrium to the ventricle. In other words, while the impulse is slowed, it is still able to get through to the ventricles. All atrial activation is eventually transmitted to the ventricles. The delay is typically due to a minor AV conduction defect occurring at or below the AV node. If the PR interval is more than 300 milliseconds, it is considered “marked” first-degree AV block and the P waves may be buried in the preceding T wave.

• Causes. There are multiple causes of first-degree AV block, including simply being a normal variant. Other causes include inferior myocardial infarction (MI), increased vagal tone (e.g., athletes), status post-cardiac surgery, myocarditis, hyperkalemia, or even medication-induced (e.g., beta-blockers, non-dihydropyridine calcium channel blocks, adenosine, digitalis, and amiodarone).
• Clinical significance. This is a benign entity that does not result in any hemodynamic instability. No specific treatment is required.

Second degree (incomplete). Second-degree or incomplete AV block occurs when there is intermittent atrial to ventricle conduction. That is, the P waves are sometimes related to the QRS complexes. It often occurs in a regular P:QRS pattern with ratios of 2:1. 3:2, 4:3, 5:4, and so forth. Second-degree AV blocks can be further classified into Mobitz type 1 (Wenckebach) or Mobitz type 2, which can be distinguished by examining the PR interval.

Second degree, Mobitz type 1 (Wenckebach). In second-degree Mobitz type 1 AV block, there is a progressive prolongation of the PR interval, which eventually culminates in a non-conducted P wave. It is often evident by clustering of QRS complexes in groups that are separated by non-conducted P waves. The greatest increase in PR interval prolongation is often between the first two beats of the cycle. While the PR interval continues to prolong with each beat of the cycle, the subsequent PR lengthening is progressively shorter. Even though the PR interval is progressively increasing in duration, the PP interval remains relatively unchanged. One way to confirm the presence of this is by noticing that the PR interval after the dropped beat is shorter than the PR interval that came before the dropped beat. In other words, the PR interval before the dropped beat is the longest of the cycle, and the PR interval after the dropped beat is the shortest as the cycle starts over.

• Mechanism. This is usually a result of a reversible conduction block at the level of the AV node. In fact, studies have shown that the site of block is likely at the crest of the AV node, where the atrium and AV node meet. There is typically a functional suppression of AV conduction. The AV nodal cells seem to progressively fatigue until they fail to conduct an impulse to the ventricles and a dropped beat occurs.
• Causes. There are multiple causes of second-degree Mobitz type 2 (Wenckebach) AV block, including reversible ischemia, myocarditis, increased vagal tone, status post-cardiac surgery, or even medications that slow AV nodal conduction (e.g., beta-blockers, non-dihydropyridine calcium channel blocks, adenosine, digitalis, and amiodarone).
• Clinical significance. Differentiating between second-degree Mobitz type 1 (Wenckebach) and Mobitz type 2 AV blocks is important as the management and treatment is different. Mobitz type 1 is often a benign rhythm. Most patients are asymptomatic, and there is tends to be minimal hemodynamic disturbance. The risk of Mobitz type 1 (Wenckebach) progressing to third-degree (complete) heart block is much lower than Mobitz type 2. Patients that are asymptomatic do not require treatment and can be monitored on an outpatient basis. Patients that are symptomatic typically respond to atropine and rarely require permanent cardiac pacing. Medication-induced impairment of AV conduction is often reversible after stopping the offending agent.

Second degree, Mobitz type 2. In second-degree Mobitz type 2 AV block, there are intermittent non-conducted P waves without warning. Unlike Mobitz type 1 (Wenckebach), there is no progressive prolongation of the PR interval; instead, the PR interval remains constant, and the P waves occur at a constant rate with unchanged P-P intervals. Because the P waves continue to occur at normal intervals, the R-R interval surrounding the dropped beat is simply a multiple of the preceding R-R interval and remains unchanged.

• Mechanism. Whereas in Mobitz type 1 there was a reversible block at the level of the AV node, in Mobitz type 2 the block occurs further along the electrical conduction system below the AV node. It can occur at the level of the His Bundle, both bundles branches, or the three fascicles (i.e., the left anterior fascicle, left posterior fascicle, and right bundle branch).
• In this case, the cells don’t progressively fatigue, but rather abruptly and unpredictably fail to conduct a supraventricular impulse. This is often the result of structural damage to the conduction system, such as from MI, fibrosis, or necrosis. Many patients have a pre-existing left bundle branch or bifascicular block, and the remaining fascicle intermittently fails to conduct causing the second degree AV block.
• Because the defect occurs below the AV node and often times distal to the His Bundle, it produces wide, bizarre-appearing QRS complexes. In the remaining cases, the defect is located within the Bundle of His, resulting in the normal, narrow QRS complexes. There can be a fixed P:QRS relationship (e.g., 2:1, 3:1) or no pattern at all.
• Causes. Common causes of second-degree Mobitz type 2 AV block include anterior MI, causing septal infarction with necrosis of the bundle branches. Other causes include idiopathic fibrosis of the conducting system, autoimmune (e.g., systemic sclerosis or systemic lupus erythematosus) or inflammatory (e.g., myocarditis, Lyme disease, or rheumatic fever) conditions, infiltrative myocardial disease (hemochromatosis, sarcoidosis, or amyloidosis), electrolyte imbalance (e.g., hyperkalemia), medication-induced (e.g., beta-blockers, non-dihydropyridine calcium channel blockers, digitalis, adenosine, or amiodarone), or status post-cardiac surgery (e.g., mitral valve repair).
• Clinical significance. Mobitz type 2 AV block can be associated with severe bradycardia and hemodynamic instability. It has a greater risk of progressing to third-degree (complete) heart block or asystole. Because the onset of dropped beats can occur abruptly and unexpectedly, hemodynamic instability and the consequential syncope and potential sudden cardiac death can occur at any moment. Thus, patients require a permanent pacemaker. While Mobitz type 1 can improve with atropine, giving atropine in the setting of Mobitz type 2 can worsen the block and increase the risk of complete heart block or asystole.

Note in cases in which every other QRS complex is dropped, there are never two consecutive PR intervals. Therefore, there is not enough information to evaluate the PR interval to further classify it as either second-degree Mobitz type 1 (Wenckebach) or Mobitz type 2 AV block. The site of block is also indeterminate.

Second degree, high-grade. High-grade AV block is a form of second-degree (incomplete) heart block that can commonly be confused with third-degree (complete) heart block. It occurs when there are two or more consecutively blocked P waves. This conduction disturbance can be particularly dangerous as it can progress to complete heart block. The anatomic region involved is almost always below the AV node as in Mobitz type 2. The P:QRS is 3:1 or higher and the ventricular rate is typically very slow. What differentiates high-grade AV block from the third-degree (complete) heart block is that there remains some relationship between the P waves and QRS complexes. In other words, there is still some AV conduction taking place.

Third-degree (complete). In third-degree, or complete, heart block there is an absence of AV nodal conduction, and the P waves are never related to the QRS complexes. In other words, the supraventricular impulses generated do not conduct to the ventricles. Instead, if ventricular conduction occurs, it is maintained by a junctional or ventricular escape rhythm. There is a complete dissociation between the atria and ventricles. The atria and ventricles conduct independent of each other. The P waves (atrial activity) are said to “march through” the QRS complexes at their regular, faster rate. The QRS complexes (ventricular activity) also occur at a regular, but slower rate. There are two independent rhythms occurring simultaneously. 

• Mechanism. Third-degree heart block is the end result of progressively worsening second-degree AV block. It can be from Mobitz type 1 if the AV nodal cells fatigue to a point in which they no longer conduct impulses through to the ventricles; or from Mobitz type 2, where there can be an abrupt and complete conduction failure throughout the His-Purkinje system. Because third-degree heart block can occur above or below the AV node, two different rhythms can take over. If it occurs above or at the crest of the AV node, a junctional rhythm will take over and drive the ventricles. The resulting QRS complexes will be narrow and occur at the intrinsic rate of the AV node (40 to 55 beats/minute). Whereas if the block occurs below the AV node, a ventricular pacemaker must take over. In such cases, the QRS complexes will be wide and at the intrinsic rate of the ventricular pacemaker (20 to 40 beats/minute).
• Causes. Complete heart block is often the result of the same causes as Mobitz type 1 and Mobitz type 2. Other causes include inferior MI, degeneration of the conduction system, and AV-nodal blocking agents such as beta-blockers, non-dihydropyridine calcium channel blockers, adenosine, digitalis, and amiodarone.
• Clinical significance. Patients with complete heart block are at great risk of developing asystole, ventricular tachycardia, and sudden cardiac death. Insertion of a permanent pacemaker is required.

AV dissociation. AV dissociation occurs when there is no relationship between the P waves and QRS complexes; however, the QRS complexes occur at a faster rate than the P rate. Unlike AV block, in which failure of an intrinsically more rapid atrial rhythm to conduct antegrade and supersede a slower ventricular rhythm is abnormal, failure of a rapid ventricular rhythm to conduct retrograde and supersede a slower atrial rhythm does not necessarily imply damage to the conducting system. In fact, AV dissociation with more rapid ventricular rates is typically due to unusual ventricular irritability.

In general, patients that present with first-degree or second-degree Mobitz type 1 AV block do not require treatment. Any provoking medications can be removed, and patients can be monitored on an outpatient basis. However, patients with higher degrees of AV block (Mobitz type 2 AV block, 3rd degree) tend to have severe damage to the conduction system. They are at a much greater risk of progressing into asystole, ventricular tachycardia, or sudden cardiac death. Hence, they require urgent admission for cardiac monitoring, backup temporary cardiac pacing, and insertion of a permanent pacemaker.[14][15][16][17]

Once diagnosed, underlying causes should be evaluated that include ischemic workup, autoimmune diseases in young patients that can cause fibrosis of the conducting system, offending medications and electrolyte disturbances such as hyperkalemia. 

Prognosis depends on the various factors that include age and other chronic medical conditions such as diabetes mellitus, chronic kidney disease, underlying heart disease, and underlying types of AV block.  

Pacemaker infection is common in the elderly, especially with underlying medical conditions. Also, sometimes it can be challenging for pacemaker patients who need other studies like MRI for diagnosing other medical conditions such as stroke.

Patients with first-degree and asymptomatic Mobitz type 1 AV block usually can continue their usual activities but should be advised to avoid medications that can prolong PR interval Patients with Mobitz type 2 and third-degree AV block should discuss with their cardiologists about the need for pacemakers. All patients should be educated on alarming symptoms of hypoperfusion such as fatigue, lightheadedness, syncope, presyncope, or angina and seek timely medical treatment 

The management of heart block is best done with an interprofessional team because if the diagnosis is missed (esp higher degrees of heart block), the condition can have significant morbidity and mortality.

Patients with heart block may be encountered by the nurse practitioner, primary care provider, internist or the emergency department physician. Except for a first-degree heart block, the rest of the patients should be referred to a cardiologist for more definitive workup. Some of these patients may require a pacemaker which can be life-saving. Following treatment, the cardiology nurse should follow up on the patients to ensure that the heart rate has normalized and the patients have no symptoms.[18]

Anytime patients with a pacemaker undergo surgery, the cardiologist should be consulted first. In some cases, the pacemaker may have to be deactivated with a magnet to prevent interference from electrocautery. After surgery, the pacemaker has to be reprogrammed. Today, most centers have a pacemaker nurse who monitors these patients for complications. Only through a combined team approach can the morbidity of heart block be decreased.