Could A Cardiac Condition Be The Cause Of Near Syncopal Spells?

Fainting spells can be caused by various factors, including abnormal heart rhythms, heart structure or function problems, and underlying medical conditions. Vasovagal syncope occurs when blood pressure drops suddenly, causing a drop in blood flow to the brain. It often occurs after standing for a while or under emotional distress. Common causes of syncope include low blood pressure, irregular heartbeats, and abrupt changes in posture.

Cardiac syncope occurs when the heart is not pumping enough blood to the brain due to an abnormal heart rhythm or structural damage to the heart. It is important to determine the cause of syncope and any underlying conditions. Some serious heart conditions, such as bradycardia, tachycardia, or blood flow obstruction, can also cause syncope.

People with known heart conditions, alcohol or drug problems, seizure disorders, diabetes, or neurological disorders are more likely to have fainting spells. Common causes of syncope include confusion, trouble breathing, fast or fluttering heartbeats, chest pain, or a weak pulse. If fainting occurs frequently and is not due to dehydration or sudden postural change, it may need to be tested for a serious heart or vascular condition.

Cardiac syncope can occur if there is a heart or blood vessel condition that affects blood flow to the brain. These conditions can include abnormal heart rhythms, cardiogenic syncope, and vasovagal syncope.

When the heart fails to generate adequate cardiac output, the brain is inadequately perfused and temporarily malfunctions, leading to syncopal events. Fainting can indicate serious heart problems and can be the first or only warning sign of a heart problem. Vasovagal syncope is caused by decreased cerebral blood flow leading to transient loss of consciousness and postural tone, associated with spontaneous episodes.

In summary, syncope is a transient condition that can be caused by various factors, including heart conditions, structural issues, and underlying medical conditions. Healthcare providers should be consulted to diagnose and manage these conditions.

Is syncope cardiac or neurological?

Syncope is a common problem, accounting for 1-3 of all emergency room visits and up to 6 of hospital admissions. Most syncopal episodes have a cardiovascular etiology, with structural or ischemic heart disease being the most prominent cause. Neurocardiogenic syncope, also known as neurally mediated syncope, is a miscommunication between the heart, blood vessels in the lower extremities, and the brain. It can be fatal, but it is not a critical disease in itself.

The mechanism of neurocardiogenic syncope is an exaggerated response to a compensatory mechanism that occurs when a person is in an upright position for a prolonged period. This triggers an exaggerated response, leading to hypotension and bradycardia. The lack of blood volume in the left ventricle results from peripheral venous pooling, which triggers a response in baroreceptors found in the aortic arch and carotid sinus, which send signals to parts of the brain controlling the vagus nerve. This profound response leads to presyncope and eventually syncope.

While not a critical disease in itself, many patients may suffer from various symptoms that vary in frequency and severity, which can lead to life-threatening injuries. Many of these patients are evaluated following a motor vehicle accident secondary to a syncopal episode while driving. It is crucial to determine the etiology of syncope so that proper treatment can be instituted and injury to the patient or others is avoided.

Can clogged arteries cause syncope?

High-grade stenosis or near occlusion of bilateral ICA is associated with stroke and transient ischemic attack (TIA) due to distal embolism or cerebral hypoperfusion. Bilateral severe stenosis of ICA can potentially cause syncope due to wide spread bilateral cerebral hypoperfusion, a rare phenomenon with minimal literature on such patients. A 67-year-old man with a history of hypertension presented with a sudden onset of syncope, collapsed, and hit his head. He woke up with bleeding from the back of his head and collapsed again.

Upon arrival at the emergency room, his heart rate was 78 beats per minute and systolic blood pressure was 136/65 mmHg. He had active glaucoma and a past history of paroxysmal atrial fibrillation, but was symptom-free for the last three years and not taking any anticoagulation medication. His past history is positive for coronary artery spasm myocardial infarction four years with normal coronary arteries on coronary angiography and catheterization.

Transthoracic echocardiogram showed normal left ventricular systolic function with slight mid diastolic abnormality. Bilateral carotid ultrasound revealed bilateral ICA stenosis of ≥ 70, predominantly smooth soft with a thin calcific component. Magnetic resonance angiogram (MRA) also revealed a short segment of 80 stenosis of the proximal right ICA and two short segments of about 60 stenosis involving the left ICA. Transfemoral carotid angiography confirmed near occlusion of the right ICA and 90 stenosis of the left ICA.

What does cardiac syncope feel like?

Vasovagal syncope is typically accompanied by a constellation of symptoms, including dizziness, nausea, pallor, tunnel vision, hearing disturbance, and profuse sweating, which collectively signal the imminent onset of syncope. The symptoms may persist following the episode due to the persistence of low blood pressure.

Is syncope related to heart failure?

Cardiac syncope occurs when the heart fails to generate enough cardiac output, causing the brain to temporarily malfunction. Bradyarrhythmias lead to this event because the heart is too slow to generate enough flow, while tachyarrhythmias force the heart to pump too fast, resulting in ineffective ventricular filling and reduced cardiac output. Mechanical obstructions to blood flow and cardiac output can also cause syncope through various mechanisms.

Chronic obstruction to forward blood flow can lead to increased ventricular size and pressure, potentially causing arrhythmias. This can also stimulate mechanoreceptors, causing secondary hypotension and bradycardia. Obstructive pathologies, such as aortic stenosis, tumors, tamponade, and congenital hypertrophic cardiomyopathy, can also follow this pathway. Infarcted or ischemic ventricular tissue can have impaired contractility, and valve rupture can result in mechanical obstruction or retrograde blood flow.

Conduction blocks and other arrhythmias can result when cardiac tissue damage is present along the conduction system. Aortic dissection can induce myocardial infarction, and pulmonary hypertension and emboli can lead to a blockade of flow through the pulmonary artery, reducing left-sided preload and cardiac output.

What causes near syncope episodes?

Syncope is a symptom caused by non-life-threatening factors like overheating, dehydration, heavy sweating, exhaustion, or sudden changes in body position. Risk factors include non-modifiable factors like male gender, which is more common in adults over 80, and family history/genetics. These factors are irreversible and cannot be changed, increasing the likelihood of syncope. These factors can trigger sudden changes in body position or sudden changes in body position, affecting blood pooling in the legs.

What is a cardiac syncope episode?

Cardiac syncope is a sudden, sudden fainting that may indicate serious heart or vascular conditions. Common causes include arrhythmia and abnormal heart rhythm, which can cause bradyarrhythmias (slow heart beats) and tachyarrhythmias (fast heart beats). Aortic dissection, a rare but life-threatening condition, is a tear in the large artery that carries blood from the heart to the body. Aortic valve stenosis, a narrowing of the valve between the heart and the aorta, can be congenital or develop in old age. These conditions can lead to a lack of oxygenated blood to the brain, causing syncope.

Is near syncope a diagnosis?

Near syncope diagnoses are often presumptive and cannot be confirmed by standard criteria, making them difficult to exclude potentially life-threatening cardiac conduction causes. Emergency department physicians often pursue extensive evaluations for patients with presyncope due to the need for prompt risk stratification and concern for cardiac etiology. The Boston Syncope Criteria accurately screens patients for risk of adverse outcomes at 30 days, recommending admission to those with high-risk factors such as symptoms of acute coronary syndrome, a cardiac or valvular disease history, family history of sudden death, signs of conduction disease, persistently abnormal vital signs, or profound volume depletion.

If the etiology is vasovagal or dehydration, patients may be discharged with close primary care provider follow-up. Other scoring systems have excluded pre- or near-syncope from their studies due to lack of uniformity in defining this population. Patients’ social situation, coping capacity, and ability to return home safely must be considered when presenting with presyncope. If discharged, patients should have close follow-up with their primary care physician or cardiologist, ideally scheduled before discharge.

What kind of heart condition causes fainting?

Fainting spells may serve as an indicator of undiagnosed cardiovascular disease, encompassing arrhythmia, structural heart defects, and functional heart disease. In children, the most common symptoms preceding a fainting episode include dizziness, lightheadedness, nausea, changes in vision, and cold, damp skin. Such indications may be indicative of the existence of cardiovascular syncope.