Table of ContentsSyncope and PresyncopePathophysiology of Neural-Mediated SyncopePathophysiology of Cardiac SyncopeClinical Presentation of SyncopeVertigoPathophysiology of Central VertigoPathophysiology of Peripheral VertigoClinical Presentation of VertigoPrehospital IdentificationConclusionReferencesSyncope and Vertigo are often used as interchangeable terms . This is inaccurate, although both are forms of dizziness. The term "dizziness" is used when a patient experiences changes in consciousness, movements, sensations and perception. The term “dizziness” can be divided into four different types: syncope/presyncope, imbalance, vertigo, and psychologically induced dizziness. These disorders are often distinguished by their subtle differences in signs and symptoms, as well as the presence or absence of environmental or medical factors (Saccomano, 2012).Say no to plagiarism. Get a tailor-made essay on “Why violent video games should not be banned”?Get the original essaySyncope and presyncopeCardiac irregularities and cerebral hypoperfusion are known to be directly linked to syncope and presyncope. Presyncope is the medical term for both the sensations of impending fainting and/or dizziness, which give up an episode of syncope. It is the actual loss of consciousness that is transient in nature. Based on the Sharpey-Schafer model, “syncope is the result of systematic acute vasodilation potentially triggered by forced contraction of an empty left ventricle” (Sharpey-Schafer, 1956). Syncope can be divided into neurally mediated syncope (NMS) and cardiac syncope/cardiac rhythm disturbances (Saccomano, 2012). Pathophysiology of Neuronal-Mediated Syncope Neuronal-mediated syncope (NMS), also known as reflex or vagal syncope, is the most common cause of syncope. in otherwise healthy patients, particularly in young women (Fu and Levine, 2014). NMS is a sudden, transient loss of consciousness resulting from an intense and abrupt decrease in blood pressure, often during changes in posture and cerebral hypoperfusion, and is known for its spontaneous recovery (Puppala, Dickinson and Benditt, 2014). This intense change in blood pressure is better known as orthostatic hypotension. The most common causes of NMS are hypotension, Valsalva maneuver, 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 blood pressure are regulated by cardiovascular reflexes and maintained within adequate margins (cardiovascular homeostasis). In the event of an alteration of these, neurocardiovascular reflex mechanisms are involved. When we stand up, blood pools toward our extremities. Within minutes, more than half a liter of blood is trapped in the veins below the heart, while circulating plasma is transferred 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). The information is relayed to the central nervous system once detected by baroreceptors. . Once the information is received, it restores blood pressure by increasing sympathetic outflow and decreasing parasympathetic tone (Fu & Levine, 2014; Malamud-Kessler et al., 2016). There are currently 6 theories regarding the specific pathophysiology of NMS. More recent studiessuggested that regardless of the large reduction in blood pressure, the prerequisite for withdrawal of sympathetic activity is no longer accurate (Malamud-Kessler et al., 2016), but further 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 cardiac disorder. Cardiac syncope is a rare and emerging condition in which patients are at high risk of cardiac arrest (Tretter & Kavey, 2013). Cardiac syncope can result from electrical malfunctions or structural disorders of the heart (Saccomano, 2012). This is most often due to tachydysrhythmias or bradycardia reducing circulating blood volume and cardiac output, leading to syncope (Saccomano, 2012). Several cardiac conditions are associated with the two main symptoms of syncope, dizziness and acute loss of consciousness, and are: sick sinus syndrome, heart block, mitral valve prolapse and aortic stenosis (Saccomano, 2012). Clinical Presentation of Syncope Neural-Mediated Syncope – characterized by prodromal symptoms approximately 1 minute before syncope and include: nausea, sweating, abdominal discomfort, pallor, sweating, yawning, and hypotension (Malamud-Kessler et al., 2016). These symptoms are usually followed by difficulty concentrating, headaches 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 hearing changes. (Malamud-Kessler et al., 2016). These patients are often adolescents and experience recurrent pre-syncopal episodes. Episodes often occur when patients quickly change positions, go from sitting to standing, or have been standing for prolonged periods. These patients do not show ECG changes (Malamud-Kessler et al., 2016). Cardiac syncope – characterized by prodromal symptoms similar to NMS, but with a reduced prevalence of dizziness, hypotension and other preceding symptoms. ECG changes are common and these patients are at significant risk of cardiac arrest (Tretter & Kavey, 2013). According to the 2013 Tretter & Kavey study, all patients who experienced cardiac syncope had either; “(1) history of syncope associated with exercise; (2) family history of heart disease; (3) an abnormal physical examination; or (4) an ECG interpreted as abnormal by a pediatric cardiologist” (Tretter & Kavey, 2013).VertigoDizziness encompasses sensations related to change in the environment or oneself. It is often described as: twists, tilts, back and forth movements, sensations of rotation and imbalance, which are often exacerbated by the actual movement. Vertigo is mainly linked to the central nervous system (uncommon) and the peripheral nervous system (common) (Saccomano, 2012). Pathophysiology of central vertigo The vestibular apparatus is responsible for transmitting information relating to spatial orientation, head position and movement, to the brain. It is also associated with motor functions responsible for maintaining posture, stabilizing the body and head during movement and balance (Tadi., 2019). It is located in the inner ear and includes three canals: utricle, saccule and semicircular. Inside these ducts are neuroepithelial hair cells. These hair cells send projections across the dividing vestibulo-cochlear nerve to the vestibular nuclei located in the dorsolateral medulla.rostral and the caudal bridge. From the vestibular nuclei, projections extend to three locations; extraocular nuclei, cerebellum and spinal cord (Tadi., 2019; Thompson & Amédée, 2009) Central vertigo and nystagmus result from a dysfunction or lesion localized to one of these vestibular structures. In these cases, the patient experiences “hallucinatory movement of the environment” and/or rotation, resulting in dizziness (Tadi., 2019; Thompson & Amedee, 2009). Underlying medical conditions are a common cause of central vertigo. Specifically; migraines, trauma, tumors and multiple sclerosis (Saccomano, 2012). However, multiple sclerosis is often the result of brainstem demyelination. Occlusion of the posteroinferior cerebellar or vertebral arteries, leading to acute lateral spinal cord syndrome, is the most well-known underlying cause of central vertigo (Thompson and Amédée, 2009). A rare cause of central vertigo is drug toxicity, especially common anticonvulsants (Tadi., 2019). Physiopathology of peripheral vertigo. Disorders that affect the labyrinth system, cranial nerve 8 and the middle ear, impair the vestibular pathway system. The labyrinth system is responsible for both balance and eye movements. When this pathway is modified, it generates a disorder of cortical integration and an overload of the pathway, thus leading to misinterpretation of the sensory data received (Saccomano, 2012; Thompson and Amédée, 2009). These events lead to peripheral dizziness, better known as benign paroxysmal positional vertigo (BPPV). The most common peripheral causes are disorders of the inner ear and labyrinth such as: benign postural vertigo, vestibular neuritis, otitis media, labyrinthitis, herpes zoster virus, viral infections, acoustic neuroma, Cogan, aminoglycoside toxicity and Ménière's disease (Saccomano, 2012; Taylor., 2019; Thompson & Amedee, 2009). Clinical presentation of VertigoCentral – characterized by gradual onset dizziness, spinning sensation, spinning environment, nystagmus, brainstem signs and symptoms, and history of migraines, tumors, or multiple sclerosis (Tadi., 2019; Thompson & Amedee, 2009). Peripheral – characterized by sudden dizziness onset of tinnitus, hearing loss , predominant vestibulocochlear signs, difficulty concentrating, nausea or vomiting (Taylor., 2019; Thompson & Amedee, 2009). Prehospital IdentificationWhen treating a patient suffering from dizziness, it is imperative to first exclude other factors, such as: drugs, alcohol, stroke, anxiety, seizures or medication use (Tadi., 2019). Once these hypotheses have been ruled out, the next step would be to: take a complete and thorough medical history; from head to toe; 12-lead ECG acquisition; Blood pressure monitoring; targeted neurological examination, including Babinski sign; targeted cardiovascular examination; and an accurate account of signs/symptoms and their frequency when possible. To rule out BPPV, the paramedic, if trained to do so, may be able to use the Dix-Hallpike maneuver if there are contraindications; cervical instability; carotid sinus syncope; vertebrobasilar insufficiency; other vascular disorders are not present. If symptoms appear, it is likely that BPPV is the cause (Tadi., 2019; Walther, 2017). If BPPV is suspected, a stroke can be excluded in the presence of a negative HiNTs exam (Tadi., 2019; Walther, 2017). . The HiNTs exam is a thorough oculomotor neurological assessment and000141