Distinct Realms of Syncope and Vertigo

Syncope and Vertigo are often used as interchangeable terms. This is inaccurate, despite both being forms of dizziness. The term ‘Dizziness’ is given when a patient experiences changes of consciousness, movement, sensation and perception. The term ‘Dizziness” can be broken into four different types; syncope/presyncope, disequilibrium, vertigo, and psychologically induced dizziness. These disorders can often be distinguished by their subtle differences in signs and symptoms, and the presence or absence of environmental or medical factors (Saccomano, 2012).

Syncope and Presyncope

Cardiac irregularities and cerebral hypoperfusion are known to directly relate to syncope and presyncope. Presyncope is the medical term describing both the sensations of imminent fainting and/or light-headedness, which forgo an episode of syncope. It is the actual loss of consciousness that is transient in nature. Based off the model by Sharpey-Schafer ‘syncope is the result of the acute systematic vasodilation potentially triggered by the forceful contraction of an empty left ventricle’ (Sharpey-Schafer, 1956). Syncope can be split into Neurally Mediated Syncope (NMS) and cardiac syncope/heart rhythm disorders (Saccomano, 2012).

Pathophysiology of Neurally Mediated Syncope

Neurally Mediated Syncope (NMS), also known as reflex or vagal syncope, is the most common cause of syncope in patients that are otherwise healthy, particularly in young women (Fu & Levine, 2014). NMS is the sudden transient loss of consciousness resulting from an intense and abrupt decrease in blood pressure, often upon changes in posture, and cerebral hypoperfusion, and is known for its spontaneous recovery (Puppala, Dickinson, & Benditt, 2014). This intense blood-pressure change is better known as orthostatic hypotension. The most common cause of NMS are hypotension, Valsalva manoeuvre, cough and dehydration (Malamud-Kessler, Estañol, Chiquete, Sentíes-Madrid, & Campos-Sánchez, 2016; Puppala et al., 2014; Saccomano, 2012; Sharpey-Schafer, 1956).

In the average human, cerebral perfusion and arterial blood pressure are regulated through cardiovascular reflexes and maintained within adequate margins (cardiovascular homeostasis). In the event these are altered, neurocardiovascular reflex mechanisms become involved. When we stand, blood pools towards our extremities. Within minutes, more than half a litre of blood becomes entrapped within the veins located below the heart, whilst circulating plasma transfers into the interstitial fluid. These changes subsequently result in a notable decrease in blood pressure, cardiac output and venous return (Fu & Levine, 2014; Malamud-Kessler et al., 2016; Saccomano, 2012).

Information is relayed to the central nervous system once detected by baroreceptors. Once the information is received, it restores blood pressure by increasing sympathetic flow and decreasing the parasympathetic tone (Fu & Levine, 2014; Malamud-Kessler et al., 2016).

There are currently 6 theories regarding the specific pathophysiology of NMS. Newer studies have suggested that, regardless of the steep reduction in arterial pressure, the pre-requisite of sympathetic activity withdrawal is no longer accurate (Malamud-Kessler et al., 2016), however more in-depth research needs to be conducted.

Pathophysiology of Cardiac Syncope

The most significant difference between NMS and Cardiac Syncope is, in most cases, the prevalence of an underlying disorder of the heart. Cardiac syncope is a rare and emergent condition where patients are at high risk of cardiac arrest (Tretter & Kavey, 2013). Cardiac syncope can result from electrical dysfunctions or structural disorders of the heart (Saccomano, 2012). This is most commonly due to tachydysrhythmias or bradycardia reducing circulating blood volume and cardiac output, resulting in the syncopal event (Saccomano, 2012).

Several cardiac disorders are associated with the two major symptoms of syncope, light-headedness and acute loss of consciousness, and are as follows; sick sinus syndrome, heart block, mitral valve prolapse and aortic stenosis (Saccomano, 2012).

Clinical Presentation of Syncope

Neurally Mediated Syncope – characterised by prodromal symptoms approximately 1 minute prior to syncope, and include; nausea, diaphoresis, abdominal discomfort, pallor, diaphoresis, yawning, and hypotension (Malamud-Kessler et al., 2016).

These symptoms are typically followed by difficulty concentrating, headache or a feeling of heaviness, and multisensory symptoms; partial or complete loss of vision, spinning sensation, tunnel vision, flashing lights, metallic taste often described as nickel, and auditory changes. (Malamud-Kessler et al., 2016).

These patients are often adolescent, and experience recurring pre-syncopal episodes. Episodes often occur when patients change position quickly, sitting to standing, or have been standing for prolonged periods of time. These patients lack ECG changes (Malamud-Kessler et al., 2016).

Cardiac Syncope – characterised by similar prodromal symptoms as NMS, but with reduced prevalence of light-headedness, hypotension, and other preceding symptoms. Changes in ECG are common, and these patients are at significant risk of cardiac arrest (Tretter & Kavey, 2013).

Based on Tretter & Kavey’s 2013 study, all patients that suffered cardiac syncope had either; “(1) history of syncope associated with exertion; (2) a concerning cardiac family history; (3) an abnormal physical examination; or (4) an ECG interpreted as abnormal by a paediatric cardiologist” (Tretter & Kavey, 2013).

Vertigo

Vertigo encompasses the sensations related to change in the environment or one’s self. It is often described as; twirling, tilting, back-and-forth motions, spinning and unbalanced feelings, which are often exacerbated by actual movement. Vertigo is primarily related to both the central nervous system (uncommon) and peripheral nervous system (common) (Saccomano, 2012).

Pathophysiology of Central Vertigo

The vestibular apparatus is responsible for the transmission of information pertaining to spatial orientation, head position and motion, to the brain. It is also associated with the motor functions responsible for maintenance of posture, body and head stabilisation during movement, and balance (Tadi., 2019). It is located within the inner ear, and is comprised of three canals; utricle, saccule and semicircular. Within these canals are neuroepithelial hair cells. These hair cells send projections through the division of the vestibulo-cochlear nerve into the vestibular nuclei located in the rostral dorsolateral medulla and caudal pons. From the vestibular nuclei the projections extend to three locations; extraocular nuclei, cerebellum and spinal cord (Tadi., 2019; Thompson & Amedee, 2009)

Central vertigo and nystagmus results from a dysfunction or lesion located on any of these vestibular structures. In these cases, the patient experiences a ‘hallucinatory motion of surroundings’ and/or spinning, resulting in dizziness (Tadi., 2019; Thompson & Amedee, 2009).

Underlying medical disorders are a common cause of central vertigo. Specifically; migraine headaches, trauma, tumours and multiple sclerosis (Saccomano, 2012). However, multiple sclerosis is often the result of brainstem demyelination. The occlusion of posterior inferior cerebellar or vertebral arteries, resulting in acute lateral medullary syndrome, is the most commonly known underlying cause of central vertigo (Thompson & Amedee, 2009). An uncommon cause of central vertigo is medication toxicity, particularly in common anticonvulsive drugs (Tadi., 2019).

Pathophysiology of Peripheral Vertigo

Disorders that affect the labyrinth system, cranial nerve 8 and middle ear, impair the vestibular pathway system. The labyrinth system is responsible for both balance and eye movements. When this pathway is altered it generates cortical integration impairment and pathway overload, consequently resulting in misinterpretation of received sensory data (Saccomano, 2012; Thompson & Amedee, 2009). These events lead to peripheral vertigo, better known as Benign Paroxysmal Positional Vertigo (BPPV).

The most common peripheral causes are inner ear and labyrinth disorders such as; benign postural vertigo, vestibular neuritis, otitis media, labyrinthitis, herpes zoster virus, viral infections, acoustic neuroma, Cogan syndrome, aminoglycoside toxicity and Ménière disease (Saccomano, 2012; Taylor., 2019; Thompson & Amedee, 2009).

Clinical Presentation of Vertigo

Central – characterised by gradual onset dizziness, spinning sensation, spinning surroundings, nystagmus, brainstem signs and symptoms, and a history of migraine headaches, tumours or multiple sclerosis (Tadi., 2019; Thompson & Amedee, 2009).

Peripheral – characterised by abrupt onset of tinnitus, hearing impairment, predominant vestibulocochlear signs, difficulty focussing, nausea or vomiting (Taylor., 2019; Thompson & Amedee, 2009).

Prehospital identification

When attending a patient with dizziness it is imperative to rule out other factors first, such as; drug, alcohol, stroke, anxiety, seiures or medication usage (Tadi., 2019). Once these have been ruled out, the next step would be to; do a complete and thorough medical history; head-to-toe; 12-Lead ECG acquisition; Blood Pressure monitoring; focused neurological exam, including Babinski sign; focused cardiovascular exam; and an accurate recount of signs/symptoms and their frequency where possible.

To rule out BPPV the paramedic, if trained to do so, may be able to utilise the Dix-Hallpike Manoeuvre if contraindications; cervical instability; carotid sinus syncope; vertebrobasilar insufficiency; other vascular disorders, are not present. If symptoms do occur, it is likely BPPV is the cause (Tadi., 2019; Walther, 2017).

In suspected BPPV, stroke can be ruled out is the presence of a negative HiNTs exam (Tadi., 2019; Walther, 2017). The HiNTs exam is a thorough and extensive three-part occulomotor neurological assessment used by medical professionals to rule out stroke, or identify lesion locality. For this assessment to be indicated, the patient must have at least one stroke risk factor. However, paramedics would require extra training to utelise and understand this assessment and result (Kattah, Talkad, Wang, Hsieh, & Newman-Toker, 2009; Tadi., 2019).

When taking medical history, ensure to inquire about any past or current inner ear and labyrinth disorders, as well as a history of migraines or tumours, as they suggest that vertigo is the likely diagnosis. Whereas, if the patient states they have a history of hypotension, had numerous episodes in the past, episodes are generally short lasting and may result in loss of consciousness/vision, or have not maintained their hydration prior to onset, it is likely syncope/pre-syncope is the cause. These patients may state that the ‘dizzy’ sensation occurs upon sudden changes in posture, and experience an aura, tunnel vision, flashing lights, metallic taste or auditory changes during an episode (Tadi., 2019).

ECG acquisition and postural blood pressure monitoring play a vital role in distinguishing between vertigo and syncope. Therefore, 12-lead acquisition and interpretation are recommended. Orthostatic hypotension (drop of 20mmHg systolic or 10mmHg diastolic) should be assessed by obtaining a blood pressure whilst lying, seating and standing. If there is a presence of orthostatic hypotension or ECG anomalies, vertigo is not likely.

Conclusion

Vertigo and syncope, although often inaccurately used as interchangeable terms for dizziness, are two very different disorders, which share several signs and symptoms. This can make it difficult to distinguish between them, particularly if an in-depth assessment has not yet been performed. There are several assessments that may assist in cultivating an accurate preliminary diagnosis, such as; Dix-Hallpike Manoeuvre; HiNTs exam; 12-Lead ECG acquisition; Blood Pressure monitoring; focused neurological exam, including Babinski sign; focused cardiovascular exam; and an accurate recount of signs/symptoms and their frequency. However, a sound understanding of each condition’s pathophysiology is required to interpret the results, and accurately identify the underlying cause.

References

1. Fu, Q., & Levine, B. D. (2014). Pathophysiology of neurally mediated syncope: Role of cardiac output and total peripheral resistance. Autonomic Neuroscience, 184, 24-26. doi:https://doi.org/10.1016/j.autneu.2014.07.004
2. Kattah, J. C., Talkad, A. V., Wang, D. Z., Hsieh, Y. H., & Newman-Toker, D. E. (2009). HINTS to diagnose stroke in the acute vestibular syndrome: three-step bedside oculomotor examination more sensitive than early MRI diffusion-weighted imaging. Stroke, 40(11), 3504-3510. doi:10.1161/strokeaha.109.551234
3. Malamud-Kessler, C., Estañol, B., Chiquete, E., Sentíes-Madrid, H., & Campos-Sánchez, M. (2016). Pathophysiology of neurally-mediated syncope. Neurología (English Edition), 31. doi:10.1016/j.nrleng.2014.04.015
4. Puppala, V. K., Dickinson, O., & Benditt, D. G. (2014). Syncope: Classification and risk stratification. Journal of Cardiology, 63(3), 171-177. doi:10.1016/j.jjcc.2013.03.019
5. Saccomano, S. J. (2012). Dizziness, vertigo, and presyncope: what's the difference? Nurse Pract, 37(12), 46-52. doi:10.1097/01.NPR.0000422206.92550.5b
6. Sharpey-Schafer, E. P. (1956). Syncope. British Medical Journal, 1(4965), 506-509. doi:10.1136/bmj.1.4965.506
7. Tadi., F. L. L. A. F. K. W. P. (2019). Central Vertigo. NCBI.
8. Taylor., B. B. R. S. (2019). Peripheral Vertigo. NCBI.
9. Thompson, T. L., & Amedee, R. (2009). Vertigo: a review of common peripheral and central vestibular disorders. The Ochsner journal, 9(1), 20-26.
10. Tretter, J. T., & Kavey, R. E. (2013). Distinguishing cardiac syncope from vasovagal syncope in a referral population. J Pediatr, 163(6), 1618-1623.e1611. doi:10.1016/j.jpeds.2013.07.023
11. Walther, L. E. (2017). Current diagnostic procedures for diagnosing vertigo and dizziness. GMS current topics in otorhinolaryngology, head and neck surgery, 16, Doc02-Doc02. doi:10.3205/cto000141