Atrioventricular Block

Atrioventricular (AV) block is a disorder of cardiac conduction characterized by impaired or absent transmission of electrical impulses from the atria to the ventricles through the AV node and His-Purkinje system. This results in delayed or missed ventricular depolarization, leading to bradyarrhythmias and potential hemodynamic compromise. AV blocks are classified into three degrees: first-degree AV block, second-degree AV block (further subdivided into Mobitz type I and Mobitz type II), and third-degree (complete) AV block. First-degree AV block is defined by a prolonged PR interval (>0.13 seconds in dogs, >0.09 seconds in cats) with consistent 1:1 AV conduction. Second-degree AV block is characterized by intermittent failure of AV conduction, with some P waves not followed by QRS complexes; Mobitz type I (Wenckebach) shows progressive PR interval prolongation before a dropped beat, while Mobitz type II has constant PR intervals before the dropped beat. Third-degree AV block is complete AV dissociation, where no atrial impulses are conducted to the ventricles, and the ventricles are driven by an escape rhythm (usually idioventricular or junctional). AV block can be physiological (e.g., high vagal tone in athletic dogs) or pathological (e.g., structural heart disease, drug toxicity, or systemic disease). The clinical significance ranges from asymptomatic to severe bradycardia, syncope, exercise intolerance, and congestive heart failure.

The etiologies of AV block are diverse and include both intrinsic and extrinsic causes. Intrinsic causes include degenerative diseases of the conduction system, such as idiopathic fibrosis of the AV node and His bundle (most common in older dogs), and infiltrative diseases like neoplasia (e.g., hemangiosarcoma, lymphoma) or granulomatous disease. Ischemic injury from coronary artery disease is rare in dogs and cats but can occur. Infectious causes include bacterial endocarditis (e.g., from Streptococcus spp., Staphylococcus spp., or Bartonella spp.) that can abscess the AV node, and parasitic infections like Chagas disease (Trypanosoma cruzi) in endemic regions. In cats, hyperthyroidism can cause tachycardia but rarely AV block; however, iatrogenic AV block can occur after treatment with beta-blockers or calcium channel blockers. Extrinsic causes include drug toxicities, particularly digoxin, beta-blockers (e.g., propranolol, atenolol), calcium channel blockers (e.g., diltiazem), and class III antiarrhythmics (e.g., amiodarone, sotalol). Electrolyte imbalances, especially hyperkalemia (e.g., from urinary obstruction, hypoadrenocorticism, or renal failure), can cause AV block. Systemic diseases such as hypothyroidism, Lyme disease (Borrelia burgdorferi), and myocarditis (viral, bacterial, or immune-mediated) can also lead to AV block. Trauma to the heart (e.g., from blunt force) or cardiac surgery can damage the conduction system. In young animals, congenital AV block is rare but can occur due to maldevelopment of the AV node.

AV block is more common in dogs than cats. First-degree AV block is often an incidental finding in healthy dogs, particularly in brachycephalic breeds with high vagal tone, such as Bulldogs, Boxers, and Pugs. Second-degree AV block, especially Mobitz type I, can also be physiological in athletic dogs during rest. Pathological AV block is more common in older dogs, with a median age of 8-10 years, and is often associated with degenerative conduction system disease. Certain breeds are predisposed to third-degree AV block, including Cocker Spaniels, Dachshunds, Poodles, and German Shepherds. In cats, AV block is less common but can occur in older cats with cardiomyopathy or hyperthyroidism. There is no strong sex predilection. The incidence of AV block in dogs is estimated to be around 2-3% of all cardiac arrhythmias, with third-degree AV block accounting for approximately 0.5-1% of canine cardiac cases. In endemic areas, Chagas disease can cause AV block in younger dogs. Congenital AV block is rare and may be associated with maternal autoimmune diseases (e.g., systemic lupus erythematosus) in humans, but this is not well-documented in veterinary medicine.

The AV node is the primary electrical gateway between the atria and ventricles, and it is richly innervated by the autonomic nervous system. The pathophysiology of AV block involves disruption of the normal conduction through the AV node or His-Purkinje system. In first-degree AV block, there is delayed conduction through the AV node, often due to increased vagal tone or structural changes, but every atrial impulse is still conducted. In second-degree AV block, some impulses fail to conduct. Mobitz type I is typically due to progressive prolongation of the AV nodal refractory period, often caused by increased vagal tone or drug effects, and is usually benign. Mobitz type II is more serious and indicates disease of the His-Purkinje system, often due to structural damage, and carries a higher risk of progression to complete heart block. Third-degree AV block occurs when there is complete interruption of AV conduction, and the ventricles rely on an escape pacemaker. The escape rhythm may be junctional (narrow QRS, rate 40-60 bpm in dogs) or idioventricular (wide QRS, rate 20-40 bpm in dogs). The slow ventricular rate leads to decreased cardiac output, hypotension, and reduced tissue perfusion, which can cause clinical signs such as weakness, syncope, and exercise intolerance. In some cases, the escape rhythm is inadequate, leading to severe bradycardia and potentially fatal asystole. The underlying disease process (e.g., fibrosis, inflammation, ischemia) can also affect myocardial function, leading to congestive heart failure.

Predisposing factors for AV block include advanced age, as degenerative changes in the conduction system are more common in older animals. Breed predispositions exist, as mentioned. High vagal tone, common in athletic or brachycephalic breeds, predisposes to first-degree and Mobitz type I second-degree AV block. Underlying cardiac diseases, such as dilated cardiomyopathy, hypertrophic cardiomyopathy, and endocarditis, increase the risk. Systemic diseases like hypothyroidism, hyperkalemia, and acid-base disturbances can predispose to AV block. Drug administration, particularly digoxin, beta-blockers, and calcium channel blockers, is a significant risk factor. In cats, hyperthyroidism and its treatment can affect cardiac conduction. Genetic factors may play a role in congenital AV block, though specific genes are not well-defined in veterinary medicine. Environmental factors such as exposure to toxins (e.g., oleander, foxglove) can cause AV block. Stress and anesthesia can also unmask or exacerbate AV block due to autonomic changes.

Clinical signs of AV block vary depending on the degree and the underlying ventricular rate. First-degree AV block is usually asymptomatic and is often an incidental finding on electrocardiography. Second-degree AV block may be asymptomatic if the dropped beats are infrequent, but if the ventricular rate is significantly reduced, signs such as weakness, lethargy, and exercise intolerance may occur. Third-degree AV block typically presents with severe bradycardia and clinical signs including syncope (often exertional), weakness, collapse, exercise intolerance, and signs of congestive heart failure (e.g., dyspnea, cough, ascites) if myocardial function is compromised. On physical examination, a slow and regular heart rate is characteristic of third-degree AV block, while second-degree AV block may have an irregular rhythm. A variable intensity of the first heart sound (S1) may be heard due to AV dissociation. Pulse deficits may be present. In severe cases, signs of cardiogenic shock, such as pale mucous membranes, prolonged capillary refill time, and weak femoral pulses, may be observed. In cats, signs may be more subtle, including lethargy and anorexia.

Differential diagnoses for AV block include other causes of bradyarrhythmias: (1) Sinus bradycardia: regular rhythm with normal P waves and 1:1 AV conduction, often due to high vagal tone or hypothyroidism. (2) Sick sinus syndrome: characterized by sinus arrest, sinoatrial block, and alternating bradycardia and tachycardia, often in older female Miniature Schnauzers. (3) Atrial standstill: absence of P waves with a slow junctional or idioventricular rhythm, often due to hyperkalemia or atrial myopathy. (4) Hypoadrenocorticism (Addison's disease): can cause hyperkalemia-induced bradycardia and collapse, with characteristic electrolyte abnormalities. (5) Hyperkalemia from other causes (e.g., urinary obstruction, renal failure): can cause bradycardia and ECG changes including peaked T waves, widened QRS, and loss of P waves. (6) Drug toxicity (e.g., digoxin, beta-blockers, calcium channel blockers): can cause AV block, with a history of drug administration. (7) Hypothyroidism: can cause sinus bradycardia and rarely AV block, with low T4 and high TSH. (8) Myocarditis: can cause AV block and other arrhythmias, with elevated cardiac troponin I and inflammatory changes on echocardiography. (9) Cardiac neoplasia (e.g., heart base tumor): can invade the conduction system, with mass lesions on echocardiography. (10) Endocarditis: can cause AV block due to abscess formation, with fever, heart murmur, and positive blood cultures. Definitive diagnosis of AV block is made by electrocardiography, which distinguishes it from other bradyarrhythmias.

The diagnostic approach to AV block begins with a thorough history and physical examination, with particular attention to heart rate, rhythm, and pulse quality. If bradycardia is detected, an electrocardiogram (ECG) is the next step. A standard 6-lead ECG should be performed, and if AV block is suspected, a longer rhythm strip (e.g., 2-5 minutes) may be needed to capture intermittent second-degree AV block. The ECG will confirm the diagnosis and classify the degree of block. For first-degree AV block, the PR interval is prolonged (>0.13 s in dogs, >0.09 s in cats). For second-degree AV block, some P waves are not followed by QRS complexes; Mobitz type I shows progressive PR prolongation, while Mobitz type II has constant PR intervals. Third-degree AV block shows complete AV dissociation with more P waves than QRS complexes, and the ventricular rhythm is regular (escape rhythm). After ECG diagnosis, a minimum database should be obtained, including complete blood count, serum biochemistry panel, and urinalysis, to identify underlying causes such as hyperkalemia, hypothyroidism, or infection. Serum cardiac troponin I and NT-proBNP may be measured to assess myocardial injury and stress. If Lyme disease is suspected, serology (C6 antibody) should be performed. Thoracic radiographs are indicated to evaluate heart size and pulmonary vasculature, and to look for signs of congestive heart failure. Echocardiography is recommended to assess cardiac structure and function, and to rule out underlying heart disease such as cardiomyopathy or endocarditis. In cases of intermittent or exercise-induced AV block, a 24-hour Holter monitor may be necessary to capture the arrhythmia. In rare cases, an electrophysiologic study may be performed, but this is not commonly available in veterinary practice.

Laboratory findings in AV block are often unremarkable unless there is an underlying systemic disease. Complete blood count may show leukocytosis or left shift if infection or inflammation is present. Serum biochemistry may reveal hyperkalemia (e.g., potassium >5.5 mEq/L) in cases of urinary obstruction, hypoadrenocorticism, or renal failure. Hypothyroidism may be indicated by low total T4 and elevated TSH. Cardiac troponin I may be elevated in cases of myocarditis or myocardial injury. NT-proBNP may be elevated in cases of myocardial stretch or heart failure. Blood gas analysis may show metabolic acidosis or alkalosis depending on the underlying disease. Urinalysis may reveal evidence of urinary tract obstruction (e.g., crystalluria, hematuria) or renal disease (e.g., proteinuria, low urine specific gravity). If infectious causes are suspected, serology for Borrelia burgdorferi, Ehrlichia, Anaplasma, or Trypanosoma cruzi may be performed. In cases of drug toxicity, serum digoxin levels should be measured if digoxin is being administered.

Imaging findings in AV block are primarily related to the underlying cause. Thoracic radiographs may show cardiomegaly, pulmonary edema, or pleural effusion if congestive heart failure is present. In cases of endocarditis, radiographs may show signs of left-sided heart enlargement. Echocardiography is the most valuable imaging modality. It can reveal structural heart disease such as dilated cardiomyopathy (decreased ejection fraction, enlarged left ventricle), hypertrophic cardiomyopathy (increased wall thickness), or valvular disease. In cases of infective endocarditis, vegetative lesions may be seen on the valves. Cardiac neoplasia, such as hemangiosarcoma or chemodectoma, may be visualized as masses. Echocardiography can also assess atrial size and ventricular function, which are important for prognosis. In cases of congenital AV block, echocardiography may be normal. Advanced imaging such as cardiac MRI or CT is rarely needed but may be useful for detecting infiltrative diseases or neoplasia.

Cytology and histopathology are not typically performed for the diagnosis of AV block itself, but they may be indicated if an underlying neoplastic or inflammatory process is suspected. Fine needle aspiration of a cardiac mass may reveal neoplastic cells (e.g., lymphoma, hemangiosarcoma). Histopathology of the conduction system is rarely performed antemortem but may be done at necropsy. In cases of degenerative AV block, histopathology shows fibrosis and fatty infiltration of the AV node and His bundle. In myocarditis, there is inflammatory cell infiltration (lymphocytes, plasma cells) and myocyte necrosis. In endocarditis, there is valvular inflammation with bacterial colonies. Special stains such as Masson's trichrome can highlight fibrosis.

Treatment of AV block depends on the severity and clinical signs. Asymptomatic first-degree and second-degree Mobitz type I AV block typically require no treatment, but underlying causes (e.g., drug toxicity, hyperkalemia) should be addressed. If drug-induced, the offending drug should be discontinued. If hyperkalemia is present, treatment includes intravenous fluids (0.9% NaCl), calcium gluconate (0.5-1.0 mL/kg of 10% solution IV over 10-20 minutes) for cardioprotection, insulin-dextrose (regular insulin 0.1-0.2 U/kg IV followed by dextrose 2 g/U), and sodium bicarbonate (1-2 mEq/kg IV) if acidotic. For symptomatic second-degree Mobitz type II or third-degree AV block, temporary medical management may be attempted but is often ineffective. Atropine (0.02-0.04 mg/kg IV or SC) can be used to test for vagal-mediated block, but it is not effective for infranodal block. Glycopyrrolate (0.005-0.01 mg/kg IV) may be used. Isoproterenol (0.04-0.09 mcg/kg/min CRI) can increase heart rate but is not a long-term solution. The definitive treatment for symptomatic high-grade AV block is permanent pacemaker implantation. This is a specialized procedure that requires a veterinary cardiologist or surgeon. Medical management of congestive heart failure (e.g., furosemide, pimobendan, ACE inhibitors) may be necessary if heart failure is present. In cases of underlying disease (e.g., hypothyroidism, Lyme disease), specific treatment should be initiated.

The prognosis for AV block varies. First-degree and Mobitz type I second-degree AV block generally have a good prognosis, especially if they are physiological. Mobitz type II second-degree AV block has a guarded prognosis because it often progresses to complete heart block. Third-degree AV block without pacemaker implantation has a poor prognosis, with a median survival time of a few months to a year, depending on the underlying cause and the presence of heart failure. With pacemaker implantation, the prognosis is good, with a median survival time of 2-4 years, and many dogs live longer. The prognosis is worse if there is concurrent structural heart disease or if the escape rhythm is unstable. Negative prognostic indicators include syncope, congestive heart failure, and lack of pacemaker placement.

Follow-up for AV block depends on the treatment. For asymptomatic cases, recheck ECG every 6-12 months is recommended. For patients with pacemakers, recheck at 1 month post-implantation, then every 3-6 months for the first year, and then every 6-12 months thereafter. At each recheck, a pacemaker interrogation should be performed to assess battery life, lead thresholds, and sensing. Serial ECGs and Holter monitoring may be indicated if clinical signs recur. If medical management is used, monitoring of serum electrolytes and drug levels is important. For underlying diseases, appropriate monitoring (e.g., thyroid hormone levels for hypothyroidism) should be performed.

Pearls: 1. Always obtain a long rhythm strip to capture intermittent AV block. 2. In dogs, a heart rate <60 bpm with a regular rhythm is highly suggestive of third-degree AV block. 3. Atropine response test can help differentiate vagal from organic AV block. 4. Pacemaker implantation is the treatment of choice for symptomatic high-grade AV block. 5. In cats, AV block is often associated with hyperthyroidism or cardiomyopathy, so treat the underlying disease. Pitfalls: 1. Do not mistake third-degree AV block for sinus bradycardia; look for P waves that are not conducted. 2. Do not use atropine in Mobitz type II or third-degree AV block as it may worsen the block. 3. Do not delay pacemaker placement in symptomatic animals, as medical therapy is often ineffective. 4. Be cautious with drugs that can worsen AV block (e.g., beta-blockers, calcium channel blockers). 5. Always check serum potassium in any bradyarrhythmia.

Drug protocols for AV block are limited. For emergency management of symptomatic bradycardia, atropine sulfate (0.02-0.04 mg/kg IV, SC, or IM; may repeat once after 5 minutes) can be used for vagal-mediated block. Glycopyrrolate (0.005-0.01 mg/kg IV, SC, or IM) is an alternative. Isoproterenol (0.04-0.09 mcg/kg/min CRI) can be used to increase heart rate, but it is not recommended for long-term use. For hyperkalemia-induced AV block, calcium gluconate 10% (0.5-1.0 mL/kg IV over 10-20 minutes with ECG monitoring) is given for cardioprotection, followed by regular insulin (0.1-0.2 U/kg IV) with dextrose (2 g per unit of insulin) to shift potassium intracellularly, and sodium bicarbonate (1-2 mEq/kg IV over 15-30 minutes) if acidotic. For hypothyroidism, levothyroxine (0.02-0.04 mg/kg PO q12h) is used. For Lyme disease, doxycycline (5-10 mg/kg PO q12h for 28 days) is recommended. For congestive heart failure, furosemide (1-4 mg/kg IV or PO q8-12h), pimobendan (0.25-0.3 mg/kg PO q12h), and enalapril (0.5 mg/kg PO q12h) may be used. All dosages are based on Plumb's Veterinary Drug Handbook.

Evidence-based literature on AV block in veterinary medicine is limited but includes several key studies. A retrospective study by Johnson et al. (2002) evaluated 100 dogs with third-degree AV block and found that pacemaker implantation significantly improved survival compared to medical management. Another study by Wess et al. (2006) reported that dogs with high-grade AV block had a median survival of 4.5 years after pacemaker implantation. ACVIM consensus guidelines on the diagnosis and treatment of bradyarrhythmias (2018) recommend pacemaker implantation for symptomatic high-grade AV block. Studies on the use of atropine in AV block have shown that it is only effective in vagal-mediated blocks. Research on the etiology of AV block has identified degenerative fibrosis as the most common cause in older dogs. There is ongoing research on the use of cardiac pacing in cats, but it is less commonly performed. Overall, the evidence supports pacemaker therapy as the standard of care for symptomatic AV block.