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CushyWoodland

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Purdue University

2024

Anna McManamey

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syncope veterinary cardiology animal health

Summary

This presentation details different types of syncope in animals, including cardiac and non-cardiac causes. It covers diagnostics, treatment, and management strategies, using examples and case studies.

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Syncope Anna McManamey, DVM, DACVIM (Cardiology) VCS 84601 January 19, 2024 Objectives Define syncope List the broad categories of syncope List the common specific causes of cardiogenic syncope Make a diagnostic plan to diagnose the cause of syncope Make an appropriate treatment plan to treat the mo...

Syncope Anna McManamey, DVM, DACVIM (Cardiology) VCS 84601 January 19, 2024 Objectives Define syncope List the broad categories of syncope List the common specific causes of cardiogenic syncope Make a diagnostic plan to diagnose the cause of syncope Make an appropriate treatment plan to treat the most likely etiology of syncope "Triage" Syncope: Definition Syncope vs Seizure Syncope A sudden loss of postural tone due to lack of cerebral oxygenation that usually has a spontaneous recovery. Seizure A burst of uncontrolled electrical activity between neurons that causes temporary abnormalities in muscle tone or movement, behaviors, sensations or states of awareness. Syncope vs Seizure SYNCOPE SEIZURE Causes of Syncope Cardiac Arrhythmogenic Cardiogenic Pulmonary hypertension Neurally Mediated Situational Vasovagal/ neurocardiogenic *The heart is VERY sensitive to vagal tone* Arrhythmogenic Syncope Diagnostics After the Rhythm Diagnosis… Why is it there? Do you treat it? Primary heart disease Electrolyte derangements Infection Neoplasia (heart or abdomen) Drug/Toxin exposure Clinically significant? Malignant Risk of sudden death Do not forget to address possible underlying causes! Arrhythmogenic Syncope - Examples Tachyarrhythmia Supraventricular tachyarrhythmia (SVT) Ventricular tachycardia (VT) Bradyarrhythmia Sick sinus syndrome (SSS) High grade atrioventricular block (AVB) Medical Treatment for TACHYarrhythmias Bradyarrhythmia: Sick Sinus Syndrome Variable heart rate (irregular) Normal AVN function and A-V association Inappropriate pauses due to disease of the SA node If no clinical signs, this is referred to as “sinus node dysfunction" (SND) Treat with oral medications if atropine responsive Otherwise, treat with pacemaker for clinical signs* Unlike high grade AVB, this rhythm does not pose a high risk for sudden death What is going on here? syncope Bradyarrhythmia: (High grade) 2nd to 3rd degree AV Block Slow heart rate Regular rhythm “narrow” QRS morphology Occasional A-V dissociation Can see various degrees of AVB in one patient Still considered at risk for sudden death (even if incidental finding) Subsidiary Pacemakers Cats: more stable escape focus between 80 and 120 bpm Dogs: Junctional pacemaker fires between 40 and 60 bpm Dogs: ventricular pacemaker fires between 20 and 40 bpm Treatment Atropine response test 0.04 mg/kg SQ | repeat ECG in 30 minutes Sinus rate should increase to 140 bpm and block should resolve if considered "responsive" Diagnostic AND therapeutic 3 sources of high vagal tone: CNS, respiratory, GI Most sinus node dysfunction is atropine responsive (at first) Most high grade AVB are NOT responsive to atropine “High grade” AVB = less than 50% of the P waves are conducted If Atropine Responsive: Treatment If no response to atropine → PACEMAKER Pacemaker implantation is definitive treatment Transvenous (RV) Epicardial (LV) Cardiogenic Syncope Cardiogenic Syncope LEFT SIDED HEART DISEASE Cannot get oxygenated blood to rest of body Examples: Valve disease (mitral valve and aortic valve insufficiency) Myocardial disease (dilated cardiomyopathy and hypertrophic cardiomyopathy phenotypes) Congenital disease (subaortic stenosis SAS) May or may not have CHF Cardiogenic Syncope RIGHT SIDED HEART DISEASE Cannot get blood to the lungs for oxygen Also causes decreased left heart filling → decreased systemic cardiac output Examples: Valve disease (tricuspid or pulmonic insufficiency) Myocardial disease (ARVC) Congenital disease (Pulmonic stenosis, tricuspid valve dysplasia) Right to left shunt (reverse PDA, PFO, ToF) The Power of the PCV/TS Right to Left shunts result in an APPROPRIATE SECONDARY POLYCYTHEMIA Reduced oxygen content to RBCs that bypass the lungs → Chronic hypoxia → Sensed by the kidney → Kidneys produce erythropoietin (EPO) → Stimulates bone marrow production of RBCs → An increased PCV in the presence of a NORMAL TS Reverse PDA Reverse PDA Patent Foramen Ovale (PFO) Reverse PDA Cardiogenic Syncope- Treatment B2 therapy Pimobendan +/- ACE inhibitor CHF therapy Furosemide, pimobendan, ACE-inhibitor, spironolactone Stenotic or obstructive lesion Atenolol LA tear Pericardiocentesis if tamponade* R → L shunt Avoid vasodilators Phlebotomy and/or hydroxyurea if PCV > 70% Pulmonary Hypertension A BRIEF REVIEW Pulmonary Hypertension Pulmonary hypertension is increased pressure within the PULMONARY VASCULAR TREE* Right heart catheterization is the gold standard Echocardiography is the most commonly used non-invasive diagnostic Cannot be assessed via systemic blood pressure Pulmonary Hypertension Classification Examples Prevalence Treatment 1. Pulmonary arterial hypertension Idiopathic PAH, cardiac shunts, pulmonary vasculitis Low Close the shunt, careful use of sildenafil, exercise restriction 2. PH due to left heart disease DCM, MVDD, congenital disease High Treat the L sided heart disease 3. PH due to respiratory disease, hypoxia, or both COPD, primary parenchymal disease (fibrosis, bronchopneumopathy), chronic altitude exposure High Sildenafil, treat the underlying disease, weight loss, environmental manipulation 4. Pulmonary emboli/thrombi/thromboemboli (PE/PT/PTE) Acute or chronic Mid-Low Anti-coagulant therapy, sildenafil 5. Parasitic disease Dirofilaria or Angiostrongylus Middle Eliminate the infection, sildenafil 6. PH with multifactorial or unclear mechanism 2 or more underlying groups, masses compressing PA Low Need to address local disease Situational/Tussive Syncope What is Situational Syncope? Syncope that is triggered by specific activity that results in increased parasympathetic tone such as: Urination Defecation Swallowing Vomiting Coughing Underlying mechanism: acceleration of rapid vagal nerve activity → bradycardia and vasodilation→ decreased cardiac output and blood pressure reduction Tussive Syncope Aka “Cough-Drop” syndrome Current theories: Coughing dramatically increases intrathoracic pressure → reduced venous return → reduced cardiac output Coughing activates baroreceptor → causes vasodilation Coughing dramatically increases intracranial pressure → cerebral hypoperfusion and hypoxia Treat the cause of the cough Dicpinigaitis, Lim, and Farmakidis. Respiratory Medicine. 2014. Situational Syncope - Management Avoid the instances that incite the events Treat the underlying condition If straining to urinate → GU work up If straining to defecate → GI work up May require medical or interventional (pacemaker) therapy Vasovagal/ Neurocardiogenic Syncope 33 Vasovagal/Neurocardiogenic/Vasodepressor /Neurally mediated bradycardia Surge in sympathetic tone that result in a n inappropriate vasodilation and bradycardia Excitement/smell In humans: sight of blood, fear, etc Quizlet These dogs had vasovagal syncope with concurrent VT ARVC typically affects dogs > 5 years of age Can make treatment challenging Vasovagal syncope is considered non-lethal Vasovagal Syncope Can affect young animals Most diagnostics are expected to be unremarkable More likely in brachycephalic breeds May need an event monitor to document the relative bradycardia following a stimulus that results in syncopal event. Syncope may worsen with beta-blockers Syncope may improve with beta-blockers* Diagnostics after GOOD History and PE: CBC Assess for anemia, polycythemia, inflammation, thrombocytosis Chemistry General organ screening and health, assess protein ECG Rule out persistent/frequent arrhythmia Thoracic radiographs Assess cardiac silhouette Assess for cardiac decompensation (CHF) UA Troponin T4 BNP Assess for proteinuria hypoT4 (DCM phenotype) hyperT4 (HCM phenotype) Blood Pressure Assess for systemic hypertension and hypotension Assess for myocyte damage Assess for myocardial stretch Echocardiogram Assess chamber pressures and function Assess for pericardial effusion Thoracic Radiographs Left atrial dilation Pulmonary venous dilation Interstitial to alveolar pattern Pulmonary Hypertension Pulmonary arterial dilation Main pulmonary artery dilation Right heart enlargement (reverse “D”) +/- Interstitial pattern Reinero. JVIMI. 2018 Left side congestive heart failure Troponin The cardiac (C) group had a significantly higher median cTnI compared to other groups Does not differentiate between arrhythmogenic and systolic function as cause However, great amount of overlap Cannot use troponin concentration alone, but may be helpful in combination with other tests Echocardiogram Allows for assessment of: Heart chamber size Heart chamber function Intracardiac shunting Heart rhythm (rhythm ECG) Pericardial effusion Pulmonary hypertension RV RA LV LA PA Challenges Animals with heart disease can also have seizures Animals with seizures can have arrhythmias Arrhythmias may be intermittent We cannot measure blood pressure continuously and chronically Boxers are at risk for vasovagal and ARVC AED can sedate animals and prevent excitement Summary Syncope should be a differential for a collapsing or “seizure-like” event Differentiating syncope from seizure relies heavily on effective history taking and ideally witnessing an event There are cardiac and non-cardiac causes of syncope The most common diagnostics include blood pressure, bloodwork (CBC, chemistry, UA+/- T4), thoracic imaging, echocardiogram, ECG/Holter/event monitor, and cardiac biomarker assessment Treatment and prognosis are determined by the etiology of syncope

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