Understanding Syncope: Causes, Diagnosis, and Management (1/3 Denta Master

Empower Yourself Against Syncope: How to Take Control of Your Health? (1/3)

introduction

Syncope is a sudden and transient loss of consciousness due to a temporary drop in blood flow to the brain. It is often associated with loss of postural tone and can be caused by various factors, including cardiac, orthostatic, and neurocardiogenic issues. The condition can be diagnosed through a thorough medical history, physical examination, and diagnostic tests such as ECG and imaging studies. Management strategies include patient education, lifestyle modifications, and, in some cases, medication or device therapy. Dental professionals should be aware of the risk factors and signs of syncope to ensure patient safety during dental procedures.

What is syncope (temporary loss of consciousness)?

Syncope is defined as a sudden and transient loss of consciousness that is secondary to a period of cerebral ischemia.
It is associated with a loss of postural tone.
The term syncope is derived from a Greek word that means “interrupt” or “to cut short.” [1]
Syncope is the medical term for fainting or passing out.
It is a temporary loss of consciousness due to a sudden, temporary drop in the amount of blood that flows to the brain.
Most cases of syncope are benign and resolve quickly without long-term consequences.
During an episode of syncope, an individual may become unconscious and limp but typically regains consciousness and alertness within a few seconds or minutes.

What are synonyms of syncope?

The term syncope has many other names.
It is also called:
- Simple faint
- Benign faint
- Vasovagal syncope
- Swoon
- Vasodepressor syncope
- Atrial bradycardia

What are the causes of syncope?

Syncope is a symptom of an underlying disease process rather than a disease itself. [2]
Although syncope mimics a death-like experience eliciting extreme consternation among both patients and their families, most syncopal events have a benign cause. [2]
Syncope occurs when there is a temporary drop in blood flow to the brain, leading to a brief loss of consciousness.
The causes of syncope can be remembered by the pneumonic CONSNOC. [3]
Cardiac: this accounts for 14% of the cases.
- It can be
  1. Structural
  2. Arrhythmia

Orthostatic : this accounts for 11% of the cases.
- It can be :
  1. Drug induced
  2. ANS failure

Neurocardiogenic: this accounts for 24% of the cases.
- It can be
  1. Vasovagal
  2. Micturition/Defecation
  3. Cough syncope
  4. Carotid hypersensitivity

Seizure
Neuropathic (Dysautonomia): this accounts for 12% of the cases.
- It can be
  - Autoimmune
  - Chronic/toxic diabetes
  - Post-viral
  - Neurodegenerative

Others: they can be mechanical or glucose-related. This accounts for 34% of the cases.
Cerebrovascular: it can be vertebrobasilar ischaemia.

What is the pathophysiology of syncope?

The pathophysiology of syncope involves the complex interplay between the circulatory system and the autonomic nervous system.
The brain needs a constant supply of glucose (through adequate caerebral blood flow) to function, and any interruption to this, even for a few seconds, can lead to loss of consciousness or syncope.
A complex mechanism involving cardiac output, systemic vascular resistance, mean arterial pressure, and intravascular volume keeps cerebral blood flow stable.
Any defect in one or more of these systems leads to decreased cerebral blood flow.
Approximately three-fourths of blood is in the venous bed, and any interference in venous return can lead to decreased cardiac output. [2]
Decreased cardiac output leads to insufficient blood flow to the brain, causing dizziness, lightheadedness, and ultimately syncope.

Circulatory System Response:

When standing, gravity causes blood to pool in the veins below heart level, reducing venous return to the heart and subsequently decreasing cardiac output.
To keep arterial pressure stable, compensatory mechanisms are activated, such as sympathetic nervous system activation via the central autonomic network (CAN).
Sympathetic outflow leads to vasoconstriction, venoconstriction, increased heart rate, and contractility to counteract the drop in blood pressure.
Leg muscle pumping enhances venous return, while the venoarterial reflex increases arterial vasoconstriction in response to venous distention.
Venous return refers to the flow of blood back to the heart from the peripheral circulation. It is a critical component of cardiac output, which is the volume of blood the heart pumps per minute.
Increased venous return plays a crucial role in maintaining adequate cardiac output and systemic arterial pressure.
A failure in this mechanism—especially during postural changes—can lead to decreased cerebral perfusion and result in syncope.

Autonomic Nervous System Involvement:

The autonomic supply to the cardiovascular system is coordinated at the CAN in the brain stem.
Pressure receptors sense changes in cardiac filling upon standing and trigger sympathetic vasomotor outflow.
Norepinephrine release causes vasoconstriction and increased heart rate to maintain blood pressure.
Orthostasis also affects renal blood flow, leading to sodium reabsorption and volume conservation through sympathetic responses and activation of the renin-angiotensin aldosterone system (RAAS).
The Renin-Angiotensin-Aldosterone System (RAAS) is a critical hormonal system that regulates blood pressure, fluid balance, and systemic vascular resistance.
It is activated in response to low blood volume or low blood pressure, leading to increased renin release from the kidneys.
Renin then converts angiotensinogen (produced by the liver) to angiotensin I, which is then converted into angiotensin II by the angiotensin-converting enzyme.
Angiotensin II has multiple effects: it causes vasoconstriction, stimulates aldosterone secretion from the adrenal glands (promoting sodium and water retention), and increases thirst.
RAAS activation typically serves as a protective mechanism against hypotension and syncope by promoting fluid retention and vasoconstriction.

Atrial Response:

Mechanoreceptors in the atrium sense decreased stretch, resulting in increased arginine vasopressin (AVP) .
Arginine vasopressin (AVP), also called antidiuretic hormone (ADH), is a peptide hormone produced in the hypothalamus and secreted by the posterior pituitary gland.
It plays a crucial role in regulating water balance, blood pressure, and vascular resistance.
AVP acts primarily on the kidneys to promote water reabsorption, which helps maintain blood volume and osmolarity.
AVP has a significant impact on cardiovascular function.
When blood volume decreases or when there is an increase in plasma osmolality (the concentration of solutes in the blood), AVP is released into circulation.
This release leads to several physiological responses:
- Vasoconstriction: AVP causes constriction of blood vessels, which increases peripheral vascular resistance and raises blood pressure.
- Water Retention: By promoting water reabsorption in the kidneys, AVP helps maintain or increase blood volume.
These mechanisms are critical for preventing hypotension (low blood pressure), which can lead to syncope.

Brain Hypoxia and Syncope:

Syncope occurs when there is a reduction in cerebral perfusion pressure, leading to brain hypoxia.
Cerebral Perfusion Pressure (CPP) is a critical physiological parameter that represents the pressure gradient driving blood flow to the brain.
An optimal CPP allows the brain to receive a constant supply of oxygen and nutrients via blood flow.
A normal range for CPP is typically between 60-80 mmHg.
Within this range, the brain can effectively regulate its blood flow to meet metabolic demands.
The temporary decrease in cerebral blood flow during syncope results in loss of consciousness until normal perfusion is restored upon recovery

What are the predisposing factors?

Predispose means: To make more likely or render susceptible.
Predisposing factors are those factors that make a person at risk of developing a problem. They increase the probability of developing a problem. [4]
In syncope, predisposing factors can either be psychogenic or non-psychogenic factors.
Psychogenic factors include:
- Anxiety
- Fright
- Pain (it can be unexpected or sudden)
- Sight of blood or surgical or other dental instruments (like a local anesthetic syringe)
- Emotional stress
- Any kind of unpleasant news. [5]
Non-psychogenic factors include:
- Exhaustion
- Poor physical condition
- Hunger from missed meal or dieting
- Hot and crowded environment
- Males between 16 and 35 years of age. [5]

What is the classification of syncope?

Based on the etiology, syncope can be classified as:
1. Cardiac syncope
2. Non-cardiac syncope
3. Undetermined syncope

Cardiac syncope: they account for 10-20% of the cases of syncope. They can be caused by:
- Due to structural abnormalities leading to decreased cardiac output. The abnormalities can be:
  - Left Ventricular Outflow Obstruction (LVOTO)
  - Right Ventricular Outflow Obstruction (RVOTO)
  - Coronary Artery Disease (CAD)
  - Aortic Dissection (AD)
    
    They account for 3–11% of the cases of cardiac syncope.
- Due to arrhythmias:
  - Tachyarrhythmias
  - Pacemaker related
    They account for 5–30% of the cases.
- Neutrally mediated syncope:
  - During and following catheterization
  - Nitrate syncope
Non-cardiac syncope: They are neurally mediated reflex syncope. They can be:
- Vasovagal syncope
- Cardiac sinus syndrome
- Situational faints like cough, defecation, micturation, swallowing syncope, etc.

Vasovagal Syncope

Vasovagal syncope is a type of reflex syncope that occurs when there is a sudden drop in blood pressure and heart rate, leading to fainting or passing out.
It is the most common form of reflex syncope and can affect individuals of all age groups.
One out of 3 people will experience vasovagal syncope at least once in their lifetime.
In individuals under 40 years old, vasovagal syncope accounts for approximately 85% of all fainting episodes, while in older adults, it comprises about half of such cases.
An overactive vagus nerve causes a sudden drop in heart rate and blood pressure, triggering the condition.
This drop results in insufficient blood flow to the brain, leading to a vasovagal syncope episode.
Common triggers for vasovagal syncope include standing for prolonged periods, intense emotions like fear or anxiety, getting overheated, and specific medical procedures like having blood drawn.
Symptoms typically occur about 30 to 60 seconds before an episode and may include lightheadedness, nausea, sweating, and feeling clammy.
During an attack, people may lose consciousness for 20 to 30 seconds before recovering quickly.
Disorientation or confusion may occur briefly after regaining consciousness.
The diagnosis of vasovagal syncope involves a healthcare provider conducting a physical exam and possibly running tests like tilt table testing or an electrocardiogram (ECG) to rule out other potential causes of fainting.
Treatment options range from self-care measures like staying hydrated and avoiding triggers to more advanced interventions such as medications or pacemakers in severe cases.

Cardiac sinus syncope

Cardiac sinus syncope, also known as Sick sinus syndrome, is a type of heart rhythm disorder that affects the heart’s natural pacemaker, the sinus node.
This condition leads to slow heartbeats, pauses between heartbeats, or irregular heart rhythms (arrhythmias).
Sick sinus syndrome is relatively uncommon and becomes more prevalent with age.
Many individuals with this condition may require a pacemaker to maintain a regular heart rhythm.
Symptoms: The symptoms of sick sinus syndrome can vary in severity and may include palpitations (rapid fluttering heartbeats), chest pain or discomfort, confusion, dizziness or lightheadedness, fainting or near-fainting episodes, fatigue, shortness of breath, and bradycardia (slower pulse).
Causes: Sick sinus syndrome occurs when the electrical signals in the heart are irregularly paced due to various factors such as age-related wear and tear of heart tissues, damage to the sinus node from surgery or scarring, underlying heart disease, inflammatory conditions affecting the heart, certain medications like those for high blood pressure or arrhythmias, Alzheimer’s disease medications, neuromuscular diseases like muscular dystrophy, obstructive sleep apnea, and rare genetic changes. [6]

cough syncope

Cough syncope, also known as post-tussive syncope, is a condition characterized by the loss of consciousness following a bout of coughing.
The phenomenon was first described in 1876 as “laryngeal vertigo” and has since been documented in numerous cases, often associated with various medical conditions.
Initially misdiagnosed as epilepsy, it is now understood to be caused primarily by the significant increase in intrathoracic pressures caused by coughing.

Patient Profile:
The typical profile of a patient experiencing cough syncope, as observed from literature reviews, is that of a middle-aged, large-framed, or overweight male with obstructive airways disease.
This demographic is believed to be more prone to generating the excessively high intrathoracic pressures that can lead to fainting episodes triggered by coughing.

Mechanism and Theories:
The exact mechanism behind cough syncope remains a subject of debate among researchers.
Several theories have been proposed to explain how the marked elevation of intrathoracic pressures during coughing can result in loss of consciousness.
One of the primary explanations for cough syncope is the intrathoracic pressure theory, which posits that intense coughing leads to significant changes in intrathoracic pressure.
When a person coughs forcefully, there is a rapid increase in intrathoracic pressure due to the contraction of respiratory muscles against a closed glottis.
This sudden elevation in pressure can have several physiological effects.
These include:
Diminished cardiac output leads to decreased systemic blood pressure and cerebral hypoperfusion.
Increased cerebrospinal fluid (CSF) pressure affects cranial vessels, reducing brain perfusion.
A concussion-like effect on the brain due to rapid changes in CSF pressure.
Recent studies suggest a neurally mediated reflex vasodepressor-bradycardia response to cough.

Management and Treatment:
Given that loss of consciousness in cough syncope directly follows a bout of coughing, eliminating the underlying cause of the cough can prevent syncopal episodes.
Therefore, managing patients with cough syncope involves thorough evaluation and treatment of any potential conditions causing the persistent cough.
Recent guidelines on cough management emphasize this approach to address the root cause and prevent further episodes.

Empower Yourself Against Syncope: How to Take Control of Your Health? (2/3)

Discover causes, symptoms, and treatments for syncope (fainting) on our comprehensive medical guide. Learn how to manage sudden loss of consciousness effectively. Get expert insights now

Learn more

Empower Yourself Against Syncope: How to Take Control of Your Health? (1/3)

Table of Contents

introduction

What is syncope (temporary loss of consciousness)?

What are synonyms of syncope?

What are the causes of syncope?