Hospital Medicine

AV block- 1st, 2nd and 3rd degree blocks

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Atrio-Ventriular Block- First, Second and Third-Degree Blocks

I. What every physician needs to know.

Atrioventricular (AV) heart block describes impairment of conduction from the atria to the ventricles via the AV junction. This impairment occurs when the atrial impulse is either delayed or does not conduct to the ventricles. The sites of block include the AV node, the bundle of His, and the bundle branches.

The anatomic site of block is either nodal or infranodal. Nodal blocks occur within the AV node and usually result in a narrow QRS complex with a ventricular escape rate greater than 40 beats per minute (bpm). Infranodal blocks originate within the bundle of His or bundle branches and often display a wide QRS complex with a slower ventricular escape rate of less than 40 bpm. A point to remember is that atropine can improve AV nodal block but will worsen an infranodal block.

The three commonly described types of AV block are 1st degree, 2nd degree and 3rd degree AV block. Second degree block is additionally divided into Mobitz type I and type II AV block. Type I is also known as Wenckebach.

First degree AV block is a bit of a misnomer. It is not a true block but instead is just a delay in conduction of the atrial impulse, resulting in an increased PR interval of greater than 200 msec.

Type I second degree AV block involves progressive PR lengthening until the QRS “drops out,” indicating the previous P wave was not conducted to the ventricles. This is typically a nodal block.

Type II second degree AV block occurs in the setting of a constant PR interval with sudden nonconduction of a P wave. Type II second degree AV block may present as a single nonconducted P wave or a repetitive pattern of nonconduction (2:1, 3:1, etc.). This block is commonly infranodal.

Be mindful of 2:1 block, which may be either type I or type II second degree AV block. A narrow QRS complex suggests nodal arrhythmia and likely type I block, while a wide complex indicates an infranodal location and type II block.

Third degree AV block occurs when P waves are not conducted to the ventricles and an ectopic, slow escape rhythm is present. In this case the atrial and ventricular impulses are not synchronous, and the atrial rate is faster than the independent ventricular rate. If the escape rhythm has a narrow QRS complex, again the origin is at or near the AV node. Conversely, a wide QRS complex suggests the block is infranodal.

The etiology of AV block is quite variable. Lenegre-Lev syndrome, also known as senile degeneration, is an age related fibrosis of the conduction system leading to AV block. Additionally, 1st degree AV block may be the result of high vagal tone in healthy individuals and is not necessary pathologic. However, it is important to remember that any AV block may be due to myocardial ischemia or infarction, particularly of the inferior or anterior walls.

Medications such as beta-blockers, calcium channel blockers, digoxin, and antiarrhythmic agents such as amiodarone may also be responsible for conduction delays. Other causes include hypothyroidism, Lyme disease, endocarditis, sarcoidosis, systemic inflammatory diseases, and genetic channelopathies.

II. Diagnostic Confirmation: Are you sure your patient has AV block?

N/A

A. History Part I: Pattern Recognition:

Asymptomatic, low grade AV block (1st degree or type I second degree) is often an incidental finding, usually reflecting prior ischemic disease or myocyte damage. If patients with 1st or 2nd degree AV block are symptomatic, they may describe palpitations, an irregular heartbeat or the feeling of “missing a beat.” However, patients with type II second degree block or 3rd degree often experience lightheadedness, syncope, angina, shortness of breath, palpitations, and fatigue. New onset AV block in the setting of acute chest pain should be considered to be myocardial infarction until proven otherwise.

B. History Part 2: Prevalence:

The occurrence of AV block increases with age and the presence of structural heart disease. Data is unclear regarding a difference between genders and among races. A family history of arrhythmia, especially at a younger age, may increase risk of developing AV block.

C. History Part 3: Competing diagnoses that can mimic AV block.

Other patterns of electrophysiology should be considered when diagnosing AV block. Interference describes the normal physiologic phenomenon in which impaired conduction is due to the refractory period generated by preceding electrical impulse and may mimic AV block. Sinus bradycardia with respiratory variation, a wandering pacemaker, sinus pauses, and sick sinus syndrome should also be included in the differential.

D. Physical Examination Findings.

Physical exam is often normal or may be significant only for bradycardia. One should listen for an irregular rhythm and a decreased intensity of the 1st heart sound. The presence of an increased a-c interval, increasing jugular venous distension, or cannon A waves (right atrium closing against a closed tricuspid valve in 3rd degree block) suggest a hemodynamically significant AV block.

E. What diagnostic tests should be performed?

N/A

1. What laboratory studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

In all patients, one should consider evaluation of electrolytes, especially calcium and potassium, digoxin level if applicable, and cardiac enzymes. Remember to repeat cardiac enzymes serially considering troponin levels may not rise for 6-12 hours after an ischemic event. Other tests to consider include blood gas analysis for pH, thyroid stimulating hormone, free T4, anti-nuclear antibody, and Lyme antibody if indicated by clinical history.

2. What imaging studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

In all patients, order serial electrocardiographies (ECGs) and a chest X-ray if the AV block is new onset. Echocardiogram should also be considered for any change in clinical condition of the patient that might be attributable to a cardiac cause. However, patients with previously known AV block do not require a new echocardiogram during hospitalization if there is no change in the pattern of block and the clinical condition is unlikely related to cardiac disease.

F. Over-utilized or “wasted” diagnostic tests associated with this diagnosis.

Echocardiograms.

III. Default Management.

N/A

A. Immediate management.

If patient has altered mental status, hypotension, shortness of breath, or chest pain likely due to AV block, place transcutaneous pacer pads and provide supplemental oxygen. Consider the use of atropine 0.5 to 1.0 milligrams (mg) intravenous (IV) if the AV block appears nodal. Check ECG, cardiac enzymes and electrolytes.

Also, one must stop AV nodal blocking agents such as beta-blockers and calcium channel blockers. If beta-blocker overdose is suspected, give glucagon. If calcium channel blocker toxicity is the potential cause, then give calcium. For digoxin toxicity, administer Digibind. Consult cardiology for possible angiogram and temporary transvenous pacemaker. Transfer the patient to the intensive care unit for continuous monitoring.

B. Physical Examination Tips to Guide Management.

Bradycardia, an irregular rhythm or a diminished S1 may be present on exam. An inability of the patient to follow instructions, crackles on pulmonary exam and cannon A waves observed within jugular venous pulsations may indicate a clinically severe AV block.

C. Laboratory Tests to Monitor Response To, and Adjustments in, Management.

Order serial cardiac enzymes and ECGs every 6 hours for at least three sets and for all changes in clinical condition. Ensure the patient has continuous cardiopulmonary monitoring. Replete the patient’s electrolytes as needed.

D. Long-term management.

Management of clinically significant heart block should include cardiology consultation. Coronary angiography may be necessary along with implantation of a permanent pacemaker. If a patient has indications for AV nodal blocking agents, it is safe and often necessary to administer these medications once a pacemaker has been implanted.

E. Common Pitfalls and Side-Effects of Management

Avoid the use of atropine if the AV block appears to be infranodal, usually evidenced by a widening of the QRS complex from baseline.

IV. Management with Co-Morbidities

N/A

A. Renal Insufficiency.

No change in standard management.

B. Liver Insufficiency.

No change in standard management.

C. Systolic and Diastolic Heart Failure

No change in standard management.

D. Coronary Artery Disease or Peripheral Vascular Disease

No change in standard management.

E. Diabetes or other Endocrine issues

No change in standard management.

F. Malignancy

No change in standard management.

G. Immunosuppression (HIV, chronic steroids, etc).

No change in standard management.

H. Primary Lung Disease (COPD, Asthma, ILD)

No change in standard management.

I. Gastrointestinal or Nutrition Issues

No change in standard management.

J. Hematologic or Coagulation Issues

No change in standard management.

K. Dementia or Psychiatric Illness/Treatment

No change in standard management.

V. Transitions of Care

A. Sign-out considerations While Hospitalized.

Be sure the patient is on continuous monitoring and have atropine and transcutaneous pacer available at the bedside for acute treatment of end-organ decompensation attributable to AV block. Consult cardiology for transvenous pacemaker if patient decompensates.

B. Anticipated Length of Stay.

Two to four days.

C. When is the Patient Ready for Discharge.

Although no clear recommendations exist regarding discharge criteria, the patient should be considered for discharge when he/she is no longer symptomatic, reversible causes have been treated, the rhythm is stable, and the permanent pacemaker has been implanted (if necessary).

D. Arranging for Clinic Follow-up

Primary care physician in 1-2 weeks of discharge. Cardiology within 3 months for evaluation of device if implanted. Optimally, the device check appointment should be with a cardiac electrophysiologist and a representative of the device manufacturer.

1. When should clinic follow up be arranged and with whom.

Primary care physician in 1-2 weeks of discharge. Cardiology within 3 months for evaluation of device if implanted. Optimally, the device check appointment should be with a cardiac electrophysiologist and a representative of the device manufacturer.

3. What tests should be ordered as an outpatient prior to, or on the day of, the clinic visit.

N/A

E. Placement Considerations.

Nothing specific to this condition. Patients should expect to return their previous level of care before hospitalization.

F. Prognosis and Patient Counseling.

Patients have an excellent prognosis after placement of permanent pacemaker, with 1/3 of patients able to survive an additional 15 years after implantation. However, it is important to remember that even just the presence of 1st degree block is associated with atrial fibrillation, heart failure, cardiovascular mortality, and all-cause mortality. Additionally, patients with permanent pacemakers should be counseled that they may not be able to undergo magnetic resonance imaging (MRI) and should carry their device cards at all times.

VI. Patient Safety and Quality Measures

A. Core Indicator Standards and Documentation.

No defined core measures.

B. Appropriate Prophylaxis and Other Measures to Prevent Readmission.

Most patients (especially if patients are age 60 years or older, require bed rest, or have heart failure) should have prophylaxis against deep venous thrombosis barring contraindications to anticoagulation. Preferred regimens are either low dose unfractionated heparin 5000 units subcutaneously (SC) every 8 hours or low molecular weight heparin, such as enoxaparin 40 mg SC daily.

Ensure the patient is aware of and understands the plan for discharge, including a review of discharge medications and follow-up dates, times and locations with a primary care physician and cardiologist for device monitoring.

What's the evidence?

Bonow, RO, Mann, DL, Zipes, DP, Libby, P, Braunwald, E. "Braunwald's Heart Disease - A Textbook of Cardiovascular Medicine". Elsevier Saunders. 2012.

Osmonov, D, Erdinler, I, Serhan, K. "Management of Patients with Drug-Induced Atrioventricular Block". Pacing and Clinical Electrophysiology. vol. 35. pp. 804-810.

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