Definition

• Endocardial splitting is a linear defect limited to the endocardial layer of the atrium (typically the left atrium) resulting from distension of the atrial wall beyond its elastic limits.
• An atrial tear may result if the split extends through the myocardium and epicardium, resulting in a full thickness defect in the atrial wall and hemorrhage into the pericardial space.

Pathophysiology

• Endocardial splitting typically results from increased left atrial volume and pressure secondary to severe mitral regurgitation and mechanical trauma from the regurgitant jet; primary endocardial degeneration may also play a role.
• If the split is incomplete, fibrin may seal the defect temporarily; this either heals as a linear depression in the endocardial surface or subsequently extends through the myocardium resulting in a complete left atrial tear.
• A left atrial tear results in peracute bleeding into the pericardial sac and severe, life-threatening hemodynamic compromise secondary to acute cardiac tamponade.
• If a tear occurs in the interatrial septum, an acquired atrial septal defect may form.
• Tearing of either atrium may also rarely occur secondary to blunt trauma, or iatrogenically during pericardiocentesis.

Systems Affected

• Cardiovascular
• Respiratory

Incidence/Prevalence

Atrial tear is a rare cause of hemorrhagic pericardial effusion in the dog encompassing approximately 2% of pericardial effusion cases.

Signalment

Signs

Causes

• Mitral valve endocardiosis
• Chordae tendinae rupture
• Cardiac neoplasia, most commonly hemangiosarcoma
• Chest trauma
• Cardiac catheterization

Risk Factors

• Severe mitral regurgitation, left atrial enlargement.
• May be precipitated by an episode of excitement, stress, or activity.

Differential Diagnosis

• Other causes of acute cardiovascular collapse or syncope
• Pericardial effusion from other causes (e.g., neoplastic and idiopathic)
• Heart failure
• Severe cardiac arrhythmias

CBC/Biochemistry/Urinalysis

• Anemia is uncommon unless pericardiocentesis is performed since volume of blood loss is relatively small.
• Hypoproteinemia is common.
• Elevations in serum lactate, metabolic acidosis.
• Increased ALT, AST in some patients.
• Prerenal azotemia; hyponatremia or other electrolyte derangements may be seen.

Other Laboratory Tests

NT-proBNP and TnI levels may be elevated.

Imaging

Diagnostic Procedures

Pathologic Findings

• Endocardial splitting is noted grossly as a pale linear depression in the atrial endocardium.
• Atrial wall tears appear as full thickness defects extending through the atrial endocardium, myocardium and epicardium; an associated thrombus may or may not be present. The caudolateral aspect of the left atrium is most commonly affected, with many tears occurring at the atrio-auricular junction.
• Hemorrhagic pericardial effusion or pericardial thrombus are seen with acute tears.
• Mitral endocardiosis characterized by thickened mitral valve leaflets with rolled edges; chordae tendinae rupture may be seen; atrial jet lesions are possible.
• Cardiomegaly with severe left atrial enlargement expected.

Appropriate Health Care

• If a left atrial tear is strongly suspected, perform pericardiocentesis only if the effusion is causing symptomatic, life-threatening cardiac tamponade, since further hemorrhage into the pericardial sac or exsanguination may occur once pericardial fluid is removed.
• If pericardiocentesis is performed, remove only enough fluid to improve clinical signs.
• Pericardiocentesis will likely be difficult given the small volume of effusion typically identified, severe cardiac enlargement, and the small size of most dogs with left atrial rupture; ultrasound guidance and continuous ECG monitoring are highly recommended.
• Best practices for management of left atrial tears have not been clearly established; however, aggressive medical management to lower left atrial pressure using afterload and preload reducers is recommended based on the author's clinical experience.
• If a fibrin clot forms over the defect, the patient may stabilize and recover.

Nursing Care

• Administer oxygen to dogs with dyspnea or signs of hemodynamic instability.
• Administer IV fluids or blood products only if evidence of hypovolemia is present; most dogs remain in a volume overloaded state and further intravascular volume expansion will increase left atrial pressure and potentially worsen tamponade.

Activity

Strict cage rest in the acute period should be followed by chronic exercise restriction.

Client Education

Left atrial tear typically accompanies advanced cardiac disease and chronic medical therapy will be necessary; though the prognosis is guarded for surviving the acute event some dogs with left atrial tear have lived more than a year after the incident.

Surgical Considerations

• Exploratory thoracotomy may be considered if hemorrhage persists or recurs but should be undertaken cautiously given the advanced state of cardiac disease typically present.
• Transcatheter septal puncture and balloon tear of the fossa ovalis may also be considered to decompress the left atrium; however, right heart failure or hypoxemia due to right-to-left shunting may result.

Drug(s) Of Choice

• Atrial tears occur secondary to elevated left atrial pressure; thus medical therapy should be focused on lowering of left atrial pressures in order to reduce continued hemorrhage into the pericardial space and permit fibrin clot formation at the site of the tear; this may be accomplished with preload (e.g., diuretics, nitroglycerin paste) and/or afterload reducers (arterial vasodilators).
• Preload and afterload reduction must be undertaken cautiously to avoid worsening of hemodynamic compromise.
• Afterload reduction may be achieved by conservative doses of sodium nitroprusside; a low starting CRI dose of 0.5–1 µg/kg/min is recommended to achieve a decrease in LA pressure without precipitating significant hypotension; blood pressure monitoring is recommended and the dose may be uptitrated as necessary every 15–30 minutes up to a maximum of 10 µg/kg/min to achieve an improvement in clinical signs and/or a reduction in blood pressure of 10–15 mmHg.
• Alternatively, amlodipine may be started at 0.1–0.2 mg/kg PO q24h; chronic amlodipine therapy may be implemented in normotensive or hypertensive animals to reduce regurgitant fraction and lower left atrial pressure.
• Diuretics should be used cautiously if needed to treat dyspnea associated with concomitant congestive heart failure (e.g., 1–2 mg/kg of furosemide IV as needed); signs of left-sided congestive heart failure may worsen as cardiac tamponade resolves due to augmentation of preload; more aggressive diuretic therapy may then be required.
• Pimobendan (0.2–0.3 mg/kg PO q12h) may result in a further reduction in left atrial pressure though studies have not specifically examined its use in the setting of left atrial rupture and the author typically delays starting inotropes for several days so as not to disrupt stability of the fibrin clot.
• Once the patient is stable, ACE inhibitors (e.g., enalapril 0.5 mg/kg q12–24h) should be implemented for chronic management of accompanying heart failure.

Precautions

• Aggressive fluid therapy is not warranted in these patients; further volume expansion may increase left atrial pressure, worsen cardiac tamponade, and contribute to hemodynamic compromise.
• Best practices for management of left atrial tear have not been clearly established; the choice of whether to perform pericardiocentesis, and whether to administer preload and/or afterload reducers should be made based on assessment of the volume status, blood pressure and clinical stability of the patient.

Possible Interactions

Sodium nitroprusside should never be administered concurrently with phosphodiesterase-V inhibitors (e.g., sildenafil or tadalafil) due to the potential for life-threatening systemic hypotension.

Patient Monitoring

• Recommend close monitoring of respiratory rate and effort, mucous membrane color and CRT, pulse quality, and heart rate; blood pressure monitoring is recommended if arterial vasodilators are implemented.
• Follow-up examination with echocardiography helps determine resolution of pericardial effusion and resorption of an atrial or pericardial clot.
• Close follow-up every 2–3 months thereafter is recommended for repeat pericardial fluid checks and medication adjustments as deemed appropriate.

Prevention/Avoidance

Recommend avoidance of strenuous physical activity and excitement.

Possible Complications

• Even if the tear seals, the patient is prone to further tears because of underlying cardiac disease.
• Most dogs have or will develop concurrent CHF.

Expected Course and Prognosis

Prognosis for survival is guarded to poor; however, some animals can do well for several months or longer with close monitoring, exercise restriction and optimal medical management of cardiac disease.

Associated Conditions

• Chronic valvular disease
• CHF
• Mainstem bronchial compression

Synonyms

• Atrial rupture
• Atrial splitting

See Also

• Atrial Septal Defect
• Atrioventricular Valve (Myxomatous) Disease
• Congestive Heart Failure
• Pericardial Effusion
• Syncope

Abbreviations

• ACE = angiotensin converting enzyme
• ALT = alanine aminotransferase
• AST = aspartate aminotransferase
• CHF= Congestive heart failure

Internet Resources

James Buchanan Cardiology Library: http://www.vin.com/MEMBERS/CMS/Misc/Default.aspx?id=7703.

Author Suzanne M. Cunningham

Consulting Editors Larry P. Tilley and Francis W.K. Smith, Jr.