Cardiac Syncope Diagnosis: A Comprehensive Guide for Healthcare Professionals

Introduction

Syncope, characterized by a sudden and temporary loss of consciousness and postural control, is a common medical condition affecting a significant portion of the population, estimated between 30% and 40%. This figure is likely underestimated due to many individuals not seeking medical attention after a syncopal episode. Syncope leads to approximately 740,000 emergency department visits and a quarter of a million hospital admissions annually in the United States alone.[1] The causes of syncope are diverse, ranging from benign vasovagal reactions to neurological, metabolic, pulmonary issues, volume depletion, and cardiac origins. While most cases of syncope are harmless, cardiac syncope is a serious concern, often indicating a potentially life-threatening underlying cardiac condition with a concerning one-year mortality rate of 30%.[2]

Cardiac syncope arises when a heart problem prevents adequate blood, oxygen, and nutrient supply to the brain, resulting in transient loss of consciousness. These cardiac issues can stem from rhythm disturbances (arrhythmias), structural heart abnormalities, or structural problems predisposing to arrhythmias. It’s estimated that cardiac syncope accounts for about 15% of all syncope cases.[3] Distinguishing cardiac syncope from other causes of syncope is a diagnostic challenge. Therefore, it is crucial for all healthcare professionals to possess a strong understanding of cardiac syncope and the essential diagnostic steps involved in its recognition and management.[4, 5] This article aims to provide a comprehensive review of Cardiac Syncope Diagnosis, etiology, pathophysiology, evaluation, and management, emphasizing the critical roles of the interprofessional healthcare team.

Etiology of Cardiac Syncope

Syncope occurs due to a temporary and global reduction in cerebral perfusion. In cardiac syncope, this hypoperfusion is a direct consequence of the heart’s inability to pump sufficient blood to the brain. This failure is typically due to either a mechanical or structural cardiac defect or an arrhythmia disrupting the heart’s electrical conduction system. Arrhythmias are considered the more frequent cause; however, structural and mechanical heart abnormalities often trigger these arrhythmias, highlighting the interconnected nature of these etiologies.

Below is an overview of common causes of cardiac syncope, which will be further elaborated in subsequent sections concerning diagnosis and management.

Structural Causes:

• Ischemic Cardiomyopathy: The most prevalent structural cardiac cause of syncope, often resulting from coronary artery disease and prior myocardial infarction.
• Valvular Abnormalities: The second most common structural cause, with aortic stenosis being the most frequent culprit, obstructing blood flow from the heart.
• Nonischemic/Dilated Cardiomyopathy: The third most common structural cause, characterized by an enlarged and weakened heart muscle.
• Hypertrophic Obstructive Cardiomyopathy (HOCM): Thickening of the heart muscle, particularly the septum, obstructing outflow and potentially causing arrhythmias.
• Aortic Dissection: A tear in the inner layer of the aorta, which can compromise blood flow and lead to syncope.
• Cardiac Tamponade: Fluid accumulation in the pericardial sac compressing the heart and impairing its function.
• Obstructive Cardiac Tumors: Tumors within the heart that can block blood flow.
• Pericardial Disease: Inflammation or constriction of the pericardium, affecting heart function.
• Pulmonary Hypertension: High blood pressure in the pulmonary arteries, straining the right ventricle and reducing cardiac output.
• Pulmonary Emboli (PE): Blood clots in the pulmonary arteries, obstructing blood flow to the lungs and indirectly affecting cardiac output and oxygenation.
• Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC): A condition where heart muscle in the right ventricle is replaced by fatty and fibrous tissue, predisposing to arrhythmias.[5, 3]

Electrical Causes (Arrhythmias):

• Tachyarrhythmias (Fast Heart Rhythms):
  • Supraventricular Tachycardia (SVT): Including atrial fibrillation, atrial flutter, paroxysmal supraventricular tachycardia (PSVT), and PSVT associated with pre-existing accessory conduction pathways like Wolff-Parkinson-White (WPW) syndrome.
  • Ventricular Tachycardia (VT): Often secondary to underlying structural heart disease or channelopathies (e.g., Brugada syndrome).
  • Pre-excitation Syndromes/Accessory Conduction Pathways: Conditions like WPW, Lown-Ganong-Levine (LGL) syndrome, Mahaim syndrome, and Breijo syndrome, which can facilitate rapid heart rhythms.
• Bradyarrhythmias (Slow Heart Rhythms):
  • Sinus Node Dysfunction: Problems with the heart’s natural pacemaker leading to slow heart rates or pauses.
  • Atrioventricular (AV) Conduction Block: Impairment of electrical signal transmission between the atria and ventricles, typically second or third-degree blocks causing significant bradycardia.
  • Pacemaker Malfunction: Failure of an implanted pacemaker to function correctly, leading to inadequate heart rate support.
• Inherited Channelopathies: Genetic disorders affecting ion channels in the heart, predisposing to arrhythmias and syncope.
  • QT Interval Disorders:
    • Long QT Syndrome (LQTS): Prolonged QT interval on ECG, increasing risk of torsades de pointes and sudden cardiac death.
      • Romano-Ward Syndrome: Autosomal dominant congenital LQTS.
      • Jervell and Lange-Nielsen Syndrome: Autosomal recessive LQTS associated with deafness.
    • Short QT Syndrome (SQTS): Abnormally short QT interval, also associated with increased arrhythmia risk.
  • Brugada Syndrome: Autosomal dominant mutation in the SCN5A gene affecting sodium channels, characterized by ST-segment elevation on ECG and increased risk of ventricular arrhythmias.
  • Catecholaminergic Polymorphic Ventricular Tachycardia (CPVT): Triggered by emotional or physical stress, caused by mutations in genes like hRyR2 (ryanodine receptor) or CASQ2 (calsequestrin-2).

Epidemiology of Cardiac Syncope

Syncope is a widespread clinical issue encountered across all demographics, irrespective of age, race, religion, or socioeconomic status. Cardiovascular disease ranks as the second most frequent cause of syncope, with arrhythmias being significantly more common than structural heart diseases. Ventricular tachycardia alone is responsible for approximately 11% of syncopal events. Cardiac syncope is notably more prevalent in older adults, with 10% to 30% of syncope cases in individuals over 60 years of age having a cardiac origin. Furthermore, cardiac syncope is observed more frequently in men compared to women.[6]

Structural cardiac diseases are more common in individuals with comorbidities such as diabetes, hypertension, hyperlipidemia, and in those who smoke. Pre-excitation syndromes, like WPW, tend to be more frequently diagnosed in women than men.[7]

Brugada syndrome shows a higher prevalence among males and individuals of Southeast Asian descent.[3] Understanding these epidemiological trends is important for risk stratification and diagnostic consideration in patients presenting with syncope.

Pathophysiology of Cardiac Syncope

The fundamental pathophysiological mechanism in all cases of cardiac syncope is the same: insufficient cardiac output leading to inadequate cerebral perfusion and temporary brain dysfunction, resulting in syncope. Bradyarrhythmias cause this by reducing the heart rate to a level where blood flow is insufficient to meet the brain’s metabolic demands. Conversely, tachyarrhythmias cause ineffective ventricular filling due to an excessively rapid heart rate, shortening the diastolic phase and ultimately reducing cardiac output.

Mechanical obstructions to blood flow and cardiac output exert similar effects through various mechanisms. Chronic obstruction to blood outflow from the heart increases ventricular size and pressure. This ventricular enlargement can heighten myocardial irritability, potentially inducing arrhythmias. Elevated ventricular pressure can also stimulate mechanoreceptors, triggering a vagal response and secondary hypotension and bradycardia. These effects are in addition to the primary issue of obstructed forward blood flow. Obstructive conditions such as aortic stenosis, cardiac tumors, tamponade, and hypertrophic cardiomyopathy, as well as myocardial infarction and ischemia, can all lead to syncope through these pathways. Infarcted or ischemic myocardial tissue suffers from impaired contractility. Damage to heart valves or chordae tendineae can lead to valve rupture, causing mechanical obstruction or retrograde blood flow. If cardiac tissue damage involves the conduction system, conduction blocks and other arrhythmias may arise. Aortic dissection can induce myocardial infarction if the dissection extends into the coronary arteries. Rupture or leakage from an aortic dissection can also reduce cardiac output due to hypovolemia or tamponade if blood enters the pericardial space. Pulmonary hypertension and pulmonary emboli impede blood flow through the pulmonary artery, reducing left-sided preload and subsequent cardiac output, alongside the primary symptom of hypoxia.[6]

Histopathology of Cardiac Syncope

Specific histopathological findings are associated with certain cardiac conditions that can cause syncope, particularly hypertrophic cardiomyopathy and arrhythmogenic right ventricular cardiomyopathy.

Hypertrophic Cardiomyopathy (HCM)

HCM is a myocardial disease characterized by asymmetrical hypertrophy of a portion of the left ventricle, often the septum. This hypertrophy reduces left ventricular filling volume and contractility due to the stiffening of the overgrown myocardium. The reduced filling volume obstructs cardiac output, diminishing blood flow to intramural coronary vessels and the rest of the body. Myocardial biopsy findings in HCM typically reveal a thickened myocardium, especially in the septum, with myocyte fiber disarray, myocardial scarring, and fibrosis, along with narrowed intramural vessels and tunica media cell dysplasia.

Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC)

ARVC is pathologically identified by the replacement of right ventricular myocytes with fibrous tissue and fat cells. Patients with ARVC typically exhibit a dilated right ventricle and may have ventricular aneurysms, which are particularly dangerous when located in the posterior basal, apical, or outflow tract regions of the heart.[8] Histopathological examination is crucial in confirming these diagnoses and differentiating them from other causes of syncope.

History and Physical Examination in Cardiac Syncope Diagnosis

In evaluating a patient with syncope for a potential cardiac etiology, a thorough clinical history is an invaluable diagnostic tool. History and physical examination alone can lead to an accurate diagnosis in approximately 45% of patients with an identifiable cause of syncope.[9] Key historical features suggesting a cardiac origin include:

• Older Age: Patients over 60 years of age are at higher risk.
• Male Sex: Cardiac syncope is more common in men.
• Pre-existing Cardiac Disease: History of any primary cardiac condition, coronary artery disease, or valvular disease.
• Pulmonary Embolism Risk Factors: Conditions such as cancer, immobility, pregnancy, or oral contraceptive use that increase the risk of pulmonary embolism.
• Exertional Syncope: Syncope occurring during or immediately after physical exertion.
• Syncope in Supine Position: Syncope occurring while lying down.
• Prodromal Palpitations or Chest Pain: Symptoms preceding syncope that suggest an arrhythmia or cardiac ischemia.
• Absence of Vagal Prodromal Symptoms: Lack of typical warning signs associated with vasovagal syncope, such as nausea, sweating, or lightheadedness.
• Family History: Family history of arrhythmias, syncope, or sudden unexplained death. [10]

The physical examination should include a careful assessment of heart rate and rhythm. Any irregularities raise suspicion of cardiac arrhythmia. Elevated respiratory rate or hypoxia may suggest pulmonary embolism. Jugular venous distention and hypotension are suggestive of obstructive mechanical cardiac etiologies like cardiac tamponade or massive pulmonary embolism. Pathological cardiac murmurs, especially new murmurs, can indicate valvular disease, hypertrophic cardiomyopathy, or obstructive intracardiac lesions. Muffled heart sounds may be heard in pericardial tamponade. Pedal edema or other signs of deep venous thrombosis increase the likelihood of pulmonary embolism.[10]

Evaluation and Diagnostic Tests for Cardiac Syncope

When cardiac syncope is suspected, initial evaluation includes a 12-lead electrocardiogram (ECG), rhythm monitoring, and potentially further investigations like echocardiography, implantable cardiac monitors, or Holter and stress testing.

Electrocardiogram (ECG)

The ECG is a critical diagnostic tool for identifying arrhythmias and underlying cardiac conditions. It can detect:

• Active Arrhythmias: Bradycardias due to conduction blocks (heart rate <50 bpm), sinus pauses (>3 seconds), or non-sustained ventricular tachycardia.
• Suggestive Findings:
  • Bifascicular Blocks: Left bundle branch block or right bundle branch block with left anterior or left posterior fascicular block.
  • Prolonged QRS Duration: QRS segments >120 milliseconds, indicating conduction delay.
  • Second-degree Mobitz Type I AV Block: Wenckebach block.
  • Complete AV Block: Third-degree AV block.
  • Premature Ventricular Contractions (PVCs): Abnormal QRS complexes indicating ventricular ectopy.
  • Early Repolarization: ST-segment elevation, which can sometimes be benign but may also be associated with increased arrhythmia risk in certain contexts.
  • Q Waves: Pathological Q waves suggesting prior myocardial infarction.
• Conditions Predisposing to Arrhythmias:
  • Wolff-Parkinson-White (WPW) Syndrome: Delta waves on ECG.
  • Brugada Syndrome: Semi-right bundle branch block pattern with coved ST-segment elevation (>2 mm) in leads V1-V3 and inverted T waves.
  • Long QT Syndrome (LQTS): Prolonged QT interval corrected for heart rate (QTc).
  • Hypertrophic Cardiomyopathy (HCM): Left atrial enlargement, left ventricular hypertrophy criteria, and potentially dagger-shaped Q waves in inferolateral leads.
  • Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC): Epsilon waves, small positive deflections at the end of the QRS complex. [10]

Laboratory Tests

Routine laboratory tests like complete blood count (CBC) and basic metabolic panel (BMP) are commonly performed in emergency department syncope evaluations but are not helpful in predicting cardiac etiology.[10] Troponin levels also have limited diagnostic utility in syncope patients. However, B-type natriuretic peptide (BNP) or N-terminal pro-BNP (NT-proBNP) measurement has shown promise in identifying cardiac syncope and patients at higher short-term risk of major adverse cardiac events (sensitivity 73%, specificity 88%).[11, 12]

Echocardiography

If cardiac syncope is suspected and no arrhythmia is detected on ECG, echocardiography is often the next most valuable diagnostic test. It directly visualizes structural heart abnormalities like valvular disease, cardiomyopathies (dilated, hypertrophic, restrictive), cardiac masses, pericardial effusion, and regional wall motion abnormalities suggesting ischemia. A retrospective study showed echocardiography confirmed the diagnosis in 48% of patients suspected of cardiac syncope and 77% of those with a specific cardiac diagnosis.[13]

Advanced Imaging: CT and MRI

Computed tomography (CT) and magnetic resonance imaging (MRI) are useful modalities for identifying structural cardiac pathologies, including pulmonary embolism (CT), cardiac masses, congenital heart disease, cardiac sarcoidosis (MRI), and arrhythmogenic right ventricular cardiomyopathy (MRI).[14, 15] Cardiac MRI is particularly valuable in visualizing myocardial tissue characteristics and detecting subtle structural abnormalities.

Rhythm Monitoring: Holter, Event Recorders, and Implantable Loop Recorders

If no arrhythmia is found on initial ECG and structural causes are ruled out or less likely, longer-term rhythm monitoring becomes crucial.

• Exercise Stress Testing: Especially useful for exertional syncope, as it can provoke exercise-induced arrhythmias or hemodynamic abnormalities. [16]
• Holter Monitor: Continuous ECG recording over 24-48 hours, recommended for patients with frequent syncope episodes.
• External Loop Recorder (Event Recorder): Patient-activated recording device worn for up to a month, useful for less frequent but recurrent symptoms.
• Implantable Cardiac Monitor (ILR): Subcutaneously implanted device that continuously monitors heart rhythm for up to 3 years, indicated for infrequent but potentially serious syncope where other tests are inconclusive. [10]

Electrophysiologic Study (EPS)

EPS is an invasive procedure involving catheter placement within the heart to assess the electrical conduction system. It can induce and identify the source of arrhythmias. While theoretically powerful, EPS has limitations in sensitivity and specificity for syncope diagnosis. It is generally reserved for patients with:

• Ischemic heart disease who might not otherwise receive an implantable cardioverter-defibrillator (ICD).
• High-risk patients where other non-invasive tests have been inconclusive.

EPS is considered diagnostic if it induces:

• Sinus bradycardia with prolonged sinus node recovery time (>525 milliseconds).
• Bundle branch block with tachycardia or His-Purkinje block (second or third degree).
• Sustained monomorphic ventricular tachycardia in patients with prior myocardial infarction.
• Recurrent symptoms with rapid supraventricular tachycardia. [17]

Treatment and Management of Cardiac Syncope

The primary goals of cardiac syncope management are to prevent morbidity, physical injuries, and economic costs associated with recurrent syncopal events, and to prevent sudden cardiac death. Treatment strategies are highly variable and tailored to address the specific underlying cardiac condition.

Management of Arrhythmias

• Sinus Node Dysfunction:
  • First, identify and discontinue any medications causing bradycardia.
  • Implantable dual-chamber pacemakers are generally recommended to prevent recurrent syncope due to sinus bradycardia. [18] However, pacemaker implantation has not consistently shown to improve overall survival, and recurrent syncope can still occur in up to 20% of patients post-implantation. [19]
• Atrioventricular Conduction System Dysfunction:
  • Pacemaker implantation is effective in preventing syncope recurrence in Mobitz type 2 second-degree or third-degree AV block. [18]
  • Biventricular pacing may be considered in patients with coexisting heart failure, reduced left ventricular ejection fraction, or prolonged QRS duration. [17]
• Fascicular Blocks:
  • Permanent pacemakers are recommended for patients with syncope and bifascicular or trifascicular bundle branch blocks, especially in the context of concerning clinical history. [18]
• Tachyarrhythmias:
  • Supraventricular Tachycardia (SVT): Catheter ablation of the accessory pathway is the definitive treatment for SVT due to accessory pathways. Medications can be used as a bridge to ablation.
  • Atrial Fibrillation: Initial management involves rate or rhythm control medications, with ablation considered if conservative therapy fails.
  • Nonsustained Ventricular Tachycardia: Beta-blockers or calcium channel blockers may be used. If ineffective, antiarrhythmic drugs can be considered, with amiodarone as a first-line option, followed by class 1A and 1C antiarrhythmics. Radiofrequency catheter ablation may be used for frequent, medication-refractory episodes.
  • Ventricular Tachycardia with Structural Heart Disease: Implantable cardiac defibrillators (ICDs) are often beneficial to reduce sudden cardiac death risk. [10] While ICDs reduce sudden death, they do not eliminate the risk of recurrent syncope or associated injuries. [17]
• Acquired QT Interval Abnormalities:
  • Discontinuation of QT-prolonging medications is typically sufficient treatment.
• Inherited Channelopathies (Long QT Syndrome, Brugada Syndrome, etc.):
  • Implantable cardiac defibrillators are the definitive management for preventing sudden cardiac death in these conditions. The decision for ICD implantation is individualized. [10]
• Implanted Pacemaker Failure:
  • Pacemaker interrogation by an electrophysiologist is necessary. Syncope may be due to battery depletion, lead oversensing, or lead underpacing, which can be addressed by device or lead replacement. [17]

Management of Structural Syncope

Treatment is directed at the specific structural heart problem:

• Aortic Stenosis: Aortic valve replacement is the definitive treatment.
• Cardiac Tumors (e.g., Atrial Myxomas): Surgical removal.
• Heart Failure or Hypertrophic Cardiomyopathy: Medical management with nitrates, diuretics, beta-blockers, and other heart failure medications.
• Coronary Artery Disease: Antiplatelet agents, anticoagulants, and revascularization procedures (angioplasty, bypass surgery) for acute coronary occlusion.
• Pulmonary Emboli: Anticoagulants and thrombolytics.
• Unknown Etiology with Known Structural Heart Disease: Evaluation for ICD implantation should be considered. [17, 10]

Driving Restrictions

All patients with cardiac syncope without definitive intervention to prevent future events should be advised not to drive. Patients with syncope have a 2 to 4 times higher risk of motor vehicle accidents compared to the general population. [10]

Differential Diagnosis of Syncope

While considering cardiac syncope, it’s crucial to differentiate it from other causes of transient loss of consciousness. Differential diagnoses include:

• Head Trauma/Concussion: Loss of consciousness directly related to head injury.

• Non-Syncopal Events:

  • Seizures: Epileptic seizures.
  • Metabolic Disturbances: Hypoglycemia, hyponatremia, hypoxia, hypocapnia.
  • Vertebrobasilar Transient Ischemic Attacks (TIAs): Transient neurological deficits due to reduced blood flow in the vertebrobasilar system.
  • Alcohol Intoxication or CNS Depressant Use: Substance-induced altered consciousness.
  • Pseudoseizures (Psychogenic Non-Epileptic Seizures – PNES): Psychological origin, mimicking seizures.
  • Psychogenic Pseudosyncope: Psychological origin, mimicking syncope, without cerebral hypoperfusion.

• Other Syncopal Etiologies (Non-Cardiac):

  • Reflex (Neurogenic) Syncope:
    • Vasovagal Syncope: Triggered by stress, fear, pain, emotional distress, sight of blood.
    • Situational Syncope: Triggered by specific actions like sneezing, laughing, coughing, urination, defecation, swallowing, or exercise.
    • Carotid Sinus Syncope: Triggered by pressure on the carotid sinus (e.g., tight collar, neck manipulation).
  • Orthostatic Hypotension:
    • Autonomic Dysfunction: Associated with conditions like Parkinson’s disease, multiple system atrophy, Lewy body dementia, diabetes, amyloidosis, spinal cord injury, or primary autonomic failure.
    • Drug-Induced Orthostatic Hypotension: Caused by diuretics, vasodilators, alcohol, antidepressants, and other medications.
    • Volume Depletion: Hemorrhage, dehydration from diarrhea, vomiting, sweating, or inadequate fluid intake. [17]

Prognosis of Cardiac Syncope

The prognosis for cardiac syncope varies greatly depending on the underlying cause and its treatability. Patients with easily treatable cardiac conditions generally have a good prognosis with appropriate management. However, patients with advanced heart failure and syncope have a significantly poorer prognosis, with a reported one-year mortality rate as high as 45%. [6] Cardiac syncope also carries a higher risk of recurrent syncopal events, with an estimated recurrence rate of 33% within 3 years. Recurrent syncope can significantly impair quality of life and increase the risk of injuries from falls, such as fractures or intracranial hemorrhage. [17]

Complications of Cardiac Syncope

While the primary focus of cardiac syncope management is preventing sudden cardiac death, syncopal events themselves can lead to immediate complications:

• Physical Injuries: Falls during syncope can result in fractures, head trauma, and other injuries.
• Economic Costs: Hospitalizations, diagnostic testing, treatments, and lost work time contribute to significant healthcare costs.

Deterrence and Patient Education for Cardiac Syncope

Patient education is crucial, particularly for those at higher risk, such as older adults and individuals with known cardiac conditions or multiple medications. Key educational points include:

• Syncope Symptoms: Educate patients about the warning signs of syncope.
• Risk Factors: Inform patients about factors that can increase syncope risk, such as certain medications (especially those causing orthostatic hypotension or QT prolongation), alcohol consumption, and dehydration.
• Importance of Seeking Medical Help: Emphasize the need to seek prompt medical attention for any syncopal episode, especially given the potentially serious nature of cardiac syncope and its association with increased mortality in advanced cardiac disease.
• Lifestyle Modifications: For patients at risk of orthostatic hypotension, advise on strategies such as adequate hydration, avoiding prolonged standing, and rising slowly from sitting or lying positions.

Pearls and Key Issues in Cardiac Syncope Diagnosis and Management

• Cardiac syncope is defined as transient loss of consciousness due to a cardiac defect, either structural or electrical, leading to insufficient cerebral perfusion.
• Patients with pre-existing cardiac abnormalities or a family history of cardiac disease or sudden death are at higher risk for cardiac syncope.
• ECG and echocardiography are essential initial diagnostic tools. Long-term rhythm monitoring may be necessary if initial tests are non-diagnostic.
• Pacemaker implantation can effectively prevent syncope due to bradyarrhythmias from sinus node dysfunction or AV conduction blocks.
• Implantable cardioverter-defibrillators (ICDs) are crucial for preventing sudden cardiac death in high-risk patients with severe heart disease or inherited channelopathies.

Enhancing Healthcare Team Outcomes in Cardiac Syncope Management

Effective management of cardiac syncope requires a collaborative interprofessional healthcare team approach. While the prognosis is favorable for patients with treatable causes, those with advanced heart failure and cardiac syncope face a high mortality risk. Recurrent syncope negatively impacts quality of life and increases the risk of injuries.

Cardiac syncope is often initially identified by primary care physicians and emergency department clinicians. Given the varied treatment approaches, timely referral for definitive workup is essential. Effective communication between emergency and primary care providers is crucial to ensure appropriate patient evaluation and management. Cardiac and emergency specialty nurses play a vital role in monitoring cardiac rhythms, promptly reporting abnormalities, and educating patients about prodromal symptoms and potential complications, enabling them to seek timely medical care. Cardiac pharmacists are essential in optimizing medication regimens and identifying potential drug-induced arrhythmias or hypotension, offering alternatives to the primary care team. A cohesive interprofessional team approach is paramount for efficient and effective diagnosis and management of cardiac syncope, ultimately improving patient outcomes and reducing mortality. [Level 5 Evidence]

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References

1. Nishijima DK, Lin AL, Weiss RE, Yagapen AN, Malveau SE, Adler DH, Bastani A, Baugh CW, Caterino JM, Clark CL, Diercks DB, Hollander JE, Nicks BA, Shah MN, Stiffler KA, Storrow AB, Wilber ST, Sun BC. ECG Predictors of Cardiac Arrhythmias in Older Adults With Syncope. Ann Emerg Med. 2018 Apr;71(4):452-461.e3. [PMC free article: PMC5866177] [PubMed: 29275946]

2. Waytz J, Cifu AS, Stern SDC. Evaluation and Management of Patients With Syncope. JAMA. 2018 Jun 05;319(21):2227-2228. [PubMed: 29872846]

3. Anderson J, O’Callaghan P. Cardiac syncope. Epilepsia. 2012 Dec;53 Suppl 7:34-41. [PubMed: 23153208]

4. Seger JJ. Syncope evaluation and management. Tex Heart Inst J. 2005;32(2):204-6. [PMC free article: PMC1163473] [PubMed: 16107115]

5. Guimarães RB, Essebag V, Furlanetto M, Yanez JPG, Farina MG, Garcia D, Almeida ED, Stephan L, Lima GG, Leiria TLL. Structural heart disease as the cause of syncope. Braz J Med Biol Res. 2018 Mar 01;51(4):e6989. [PMC free article: PMC5856435] [PubMed: 29513795]

6. Arthur W, Kaye GC. The pathophysiology of common causes of syncope. Postgrad Med J. 2000 Dec;76(902):750-3. [PMC free article: PMC1741836] [PubMed: 11085764]

7. Ceresnak SR, Dubin AM. Wolff-Parkinson-White syndrome (WPW) and athletes: Darwin at play? J Electrocardiol. 2015 May-Jun;48(3):356-61. [PubMed: 25722079]

8. Vettor G, Zorzi A, Basso C, Thiene G, Corrado D. Syncope as a Warning Symptom of Sudden Cardiac Death in Athletes. Cardiol Clin. 2015 Aug;33(3):423-32. [PubMed: 26115828]

9. Linzer M, Yang EH, Estes NA, Wang P, Vorperian VR, Kapoor WN. Diagnosing syncope. Part 1: Value of history, physical examination, and electrocardiography. Clinical Efficacy Assessment Project of the American College of Physicians. Ann Intern Med. 1997 Jun 15;126(12):989-96. [PubMed: 9182479]

10. Shen WK, Sheldon RS, Benditt DG, Cohen MI, Forman DE, Goldberger ZD, Grubb BP, Hamdan MH, Krahn AD, Link MS, Olshansky B, Raj SR, Sandhu RK, Sorajja D, Sun BC, Yancy CW. 2017 ACC/AHA/HRS Guideline for the Evaluation and Management of Patients With Syncope: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. J Am Coll Cardiol. 2017 Aug 01;70(5):e39-e110. [PubMed: 28286221]

11. Thiruganasambandamoorthy V, Ramaekers R, Rahman MO, Stiell IG, Sikora L, Kelly SL, Christ M, Claret PG, Reed MJ. Prognostic value of cardiac biomarkers in the risk stratification of syncope: a systematic review. Intern Emerg Med. 2015 Dec;10(8):1003-14. [PubMed: 26498335]

12. Tanimoto K, Yukiiri K, Mizushige K, Takagi Y, Masugata H, Shinomiya K, Hosomi N, Takahashi T, Ohmori K, Kohno M. Usefulness of brain natriuretic peptide as a marker for separating cardiac and noncardiac causes of syncope. Am J Cardiol. 2004 Jan 15;93(2):228-30. [PubMed: 14715356]

13. Recchia D, Barzilai B. Echocardiography in the evaluation of patients with syncope. J Gen Intern Med. 1995 Dec;10(12):649-55. [PubMed: 8770716]

14. Tandri H, Calkins H. MR and CT imaging of Arrhythmogenic Cardiomyopathy. Card Electrophysiol Clin. 2011 Jun 01;3(2):269-280. [PMC free article: PMC3085887] [PubMed: 21552378]

15. Sparrow PJ, Merchant N, Provost YL, Doyle DJ, Nguyen ET, Paul NS. CT and MR imaging findings in patients with acquired heart disease at risk for sudden cardiac death. Radiographics. 2009 May-Jun;29(3):805-23. [PubMed: 19448117]

16. Kapoor WN. Evaluation and outcome of patients with syncope. Medicine (Baltimore). 1990 May;69(3):160-75. [PubMed: 2189056]

17. Task Force for the Diagnosis and Management of Syncope. European Society of Cardiology (ESC). European Heart Rhythm Association (EHRA). Heart Failure Association (HFA). Heart Rhythm Society (HRS). Moya A, Sutton R, Ammirati F, Blanc JJ, Brignole M, Dahm JB, Deharo JC, Gajek J, Gjesdal K, Krahn A, Massin M, Pepi M, Pezawas T, Ruiz Granell R, Sarasin F, Ungar A, van Dijk JG, Walma EP, Wieling W. Guidelines for the diagnosis and management of syncope (version 2009). Eur Heart J. 2009 Nov;30(21):2631-71. [PMC free article: PMC3295536] [PubMed: 19713422]

18. Epstein AE, DiMarco JP, Ellenbogen KA, Estes NA, Freedman RA, Gettes LS, Gillinov AM, Gregoratos G, Hammill SC, Hayes DL, Hlatky MA, Newby LK, Page RL, Schoenfeld MH, Silka MJ, Stevenson LW, Sweeney MO, Tracy CM, Epstein AE, Darbar D, DiMarco JP, Dunbar SB, Estes NA, Ferguson TB, Hammill SC, Karasik PE, Link MS, Marine JE, Schoenfeld MH, Shanker AJ, Silka MJ, Stevenson LW, Stevenson WG, Varosy PD., American College of Cardiology Foundation. American Heart Association Task Force on Practice Guidelines. Heart Rhythm Society. 2012 ACCF/AHA/HRS focused update incorporated into the ACCF/AHA/HRS 2008 guidelines for device-based therapy of cardiac rhythm abnormalities: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society. J Am Coll Cardiol. 2013 Jan 22;61(3):e6-75. [PubMed: 23265327]

19. Sgarbossa EB, Pinski SL, Jaeger FJ, Trohman RG, Maloney JD. Incidence and predictors of syncope in paced patients with sick sinus syndrome. Pacing Clin Electrophysiol. 1992 Nov;15(11 Pt 2):2055-60. [PubMed: 1279599]

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Disclosures:

Disclosure: Esther Mizrachi declares no relevant financial relationships with ineligible companies.

Disclosure: Kranthi Sitammagari declares no relevant financial relationships with ineligible companies.