First Degree Atrioventricular Block (First Degree Heart Block)
Definition of Atrioventricular Block
Atrioventricular Block: delayed/intermittent/completely absent transmission of the impulse from atria to the ventricles (either transiently or permanently) due to anatomical/functional impairment of the cardiac conduction system
Epidemiology: occurs in younger patients (may be hereditary)
Physiology: progressive, fibrotic, sclerodegenerative disease of the conduction system
Clinical: frequently associated with slow progression to complete heart block
Lev’s Disease
Epidemiology: occurs in older patients
Physiology: fibrosis/calcification extending from any of the left-sided fibrous structures adjacent to the conduction system into the conduction system itself
Fibrosis of the Top of the Muscular Septum: commonly causes right bundle branch block with left anterior fascicular block
Calcification of the Mitral Valve Ring or the Central Fibrous Body: may be the most common cause of complete heart block with a narrow QRS complex
Aortic Valve Calcification: may invade the bundle of His, right bundle branch, left bundle branch, and/or left anterior fascicle -> QRS complex may be prolonged
Hyperthyroidism (Severe)/Thyrotoxic Periodic Paralysis (see Hyperthyroidism, [[Hyperthyroidism]])
Hypothyroidism (Severe) (see Hypothyroidism, [[Hypothyroidism]])
Iatrogenic
Alcohol (Ethanol) Septal Ablation for Hypertrophic Cardiomyopathy (see Hypertrophic Cardiomyopathy, [[Hypertrophic Cardiomyopathy]])
Epidemiology: complete heart block occurs in 14-22% of cases
Physiology: ethanol infusion into the first septal perforating branch of the left anterior descending (LAD) coronary artery -> infarction/thinning of the proximal interventricular septum
Cardiac Surgery
Epidemiology: complete heart block occurs in 1-5.7% of cases
Risk Factors for Post-Cardiac Surgery Complete Heart Block
Aortic Valve Annular Calcification
Aortic Valve Surgery
Bicuspid Aortic Valve
Female Gender
Pre-Existing Conduction System Disease (RBBB or LBBB)
Procedures
Aortic Valve Replacement of a Calcified Aortic Valve
Left Anterior Descending (LAD) Coronary Artery Stenting
Epidemiology: rare
Physiology: due to stent-related occlusion of septal perforator artery -> septal infarction
Swan-Ganz Catheter Interference with Right Bundle Branch Conduction in Setting of Pre-Existing Left Bundle Branch Block (LBBB) (see Swan-Ganz Catheter, [[Swan-Ganz Catheter]])
Trans-Catheter Aortic Valve Replacement (TAVR) (see Aortic Stenosis, [[Aortic Stenosis]])
Epidemiology: approximately 33% of patients require a permanent pacemaker within 30 days of TAVR
There may be a higher rate of atrioventricular block with self-expanding implanted aortic valves, as compared to balloon expandable versions
Predictors of Post-TAVR Atrioventricular Block
Pre-existing cardiac conduction disturbance
Narrow left ventricular outflow tract
Increased severity of mitral annular calcification appear to be predictors of this complication
Trans-Catheter Closure of Ventricular Septal Defect (VSD) (see Ventricular Septal Defect, [[Ventricular Septal Defect]])
Amplatzer Ventricular Septal Defect Occluder: likely due to the right ventricular retention disk overlapping the ventricular conduction system as it passes above or anterosuperiorly to the ventricular septal defect
Drugs/Toxins
Adenosine (Adenocard) (see Adenosine, [[Adenosine]])
Amiodarone (Cordarone) (see Amiodarone, [[Amiodarone]])
Diltiazem (Cardizem, Tiazac, Dilt-CD) (see Diltiazem, [[Diltiazem]])
Verapamil (Isoptin, Verelan, Verelan PM, Calan, Bosoptin, Covera-HS) (see Verapamil, [[Verapamil]]): probably the most common calcium channel blocker associated with atrioventricular blocks
Physiology: atrioventricular nodal blockade, since calcium channels are especially concentrated in the sinoatrial and atrioventricular nodes within the heart
Digitalis Intoxication (see Digitalis, [[Digitalis]])
Physiology: digitalis is a cardiac glycoside -> inhibits myocardial Na+/K+ ATPase and increases vagal activity
Physiology: digoxin is a cardiac glycoside -> inhibits myocardial Na+/K+ ATPase and increases vagal activity
Disopyramide (Norpace) (see Disopyramide, [[Disopyramide]])
Physiology: modulates the sodium channel
Clinical: may produce block in the more distal His-Purkinje system
Mad Honey Intoxication (see Mad Honey, [[Mad Honey]])
Physiology: grayanotoxin-contaminated honey made from Rhododendron Ponticum and other plant species from the Ericaceae and Sapindaceae families -> increased cardiac sodium channel permeability
Nerium Oleander Intoxication (see Nerium Oleander, [[Nerium Oleander]])
Physiology: contains oleandrin and other less well-studied cardiac glycosides
Procainamide (Pronestyl) (see Procainamide, [[Procainamide]])
Physiology: modulates the sodium channel
Clinical: may produce block in the more distal His-Purkinje system
Quinidine (Quinaglute, Quinidex) (see Quinidine, [[Quinidine]])
Physiology: modulates the sodium channel
Clinical: may produce block in the more distal His-Purkinje system
Endocarditis with Valve Ring Abscess (see Endocarditis, [[Endocarditis]])
Mitochondrial Myopathy
Myocardial Bridging
Nail-Patella Syndrome
Neonatal Lupus Syndrome
Physiology: trans-placental passage of anti-Ro/SSA or anti-La/SSB antibodies from mother
Phase IV Block (Bradycardia-Related Block)
Physiology
First Degree Atrioventricular Block with Normal QRS Duration
Conduction Delay in Atrium, AV Node, Bundle of His, or Infra-Hisian Specialized Conduction System: conduction delay in more than one of these sites has been reported to occur in 20-80% of cases
Atrial Site of Conduction Delay: site of conduction delay in 3% of first degree block cases
Bundle of His Site of Conduction Delay: slowed conduction in this site can result in split His potentials, but the PR interval is rarely prolonged
Disopyramide (Norpace) (see Disopyramide, [[Disopyramide]])
Procainamide (Pronestyl) (see Procainamide, [[Procainamide]])
Quinidine (Quinaglute, Quinidex) (see Quinidine, [[Quinidine]])
Infra-Hisian Specialized Conduction System Site of Conduction Delay (Bundle Branches, Fascicles, Terminal Purkinje Fibers): conduction is equally slowed in both the right and left conducting systems in these cases (as the PR interval is normal if one bundle is intact)
Disopyramide (Norpace) (see Disopyramide, [[Disopyramide]])
Procainamide (Pronestyl) (see Procainamide, [[Procainamide]])
Quinidine (Quinaglute, Quinidex) (see Quinidine, [[Quinidine]])
First Degree Atrioventricular Block with Wide QRS Duration
Conduction Delay in AV Node, Bundle of His, or Infra-Hisian Specialized Conduction System: 66% of cases have conduction delay in at least 2 sites (Example: as RBBB usually has a normal PR interval, when the PR interval is prolonged, there must also be a second site of delay in the AV node, His bundle, or left bundle branch)
AV Nodal Site of Conduction Delay: occasional site of conduction delay in these cases
Bundle of His Site of Conduction Delay: occasional site of conduction delay in these cases
Infra-Hisian Specialized Conduction System Site of Conduction Delay (Bundle Branches, Fascicles, Terminal Purkinje Fibers): most common site of conduction delay in these cases
Diagnosis
Electrocardiogram (EKG) (see Electrocardiogram, [[Electrocardiogram]])
Definition of First Degree Atrioventricular Block: PR interval prolonged >0.2 sec (200 msec)
Variable Effect in Patient with Atrioventricular Block: since vagal tone slows AV nodal conduction but has little effect on the infranodal conduction system
AV Nodal Site of Conduction Delay: atropine enhances AV nodal conduction and shorten the PR interval
Infranodal Site of Conduction Delay: atropine will accelerate the SA node firing (and heart rate), encroaching on the refractory period and exacerbating the conduction delay
Exercise
Increased Adrenergic Tone During Exercise Increases the Sinus Rate and Accelerates AV Nodal Conduction: therefore, results in similar effects to atropine testing
Vagal Maneuvers
Vagal Maneuvers Generally Act to Slow AV Nodal Conduction: however, this effect may be obscured since the sinus rate is also slowed (which allows more time for the AV node and the infranodal conduction system to recover from the refractory period and to conduct more normally)
Electrophysiologic (EP) Study
His Bundle Electrocardiography: most accurate means of determining the site of conduction delay
Clinical Manifestations
Cardiovascular Manifestations
Isolated First Degree Atrioventricular Block with No Apparent Heart Disease
Clinical: asymptomatic
First Degree Atrioventricular Block with “Pacemaker Syndrome”
Physiology: first degree atrioventricular block associated with loss of atrioventricular synchrony
Contraction Against a Closed Mitral Valve
Atrial Contraction Occurring Shortly after Ventricular Systole with Associated Incomplete Atrial Filling
Evaluation of New Onset First Degree Atrioventricular Block
Evaluate for Other Associated Cardiac Disease
Muscular Dystrophy-Related Cardiomyopathy
Infiltrative Cardiomyopathy
Other Dilated Cardiomyopathies
Eliminate Other Etiologies of AV Nodal Block
AV Nodal Blocking Medications
Myocardial Ischemia
Determination of Site of Conduction Disturbance
First Degree Atrioventricular Block with PR Interval >300 msec (Especially with Normal QRS Duration)
Suggests an AV Nodal Site of Conduction Delay: no further evaluation is required
First Degree Atrioventricular Block with Wide QRS
Suggests Significant Possibility That the Site of Conduction Delay is Below the AV Node: due to the unpredictable progression to second/third degree atrioventricular block, His bundle electrocardiography should be considered
HV Interval Prolongation >100 msec: permanent pacemaker placement is indicated
Indications for Permanent Pacemaker in First Degree Atrioventricular Block
First Degree Atrioventricular Block with Wide QRS and His Bundle Electrocardiography Demonstrating HV Interval Prolongation >100 msec: probable indication for permanent pacemaker placement (although this is controversial)
First Degree Atrioventricular Block with “Pacemaker Syndrome”
First Degree Atrioventricular Block with Concurrent Neuromuscular Disease: due to the unpredictable progression of atrioventricular conduction disturbances
