Topic > Distinct Realms of Syncope and Vertigo

Index Syncope and PresyncopePathophysiology of Neuromediated SyncopePathophysiology of Cardiac SyncopeClinical Presentation of SyncopeVertigoPathophysiology of Central VertigoPathophysiology of Peripheral VertigoClinical Presentation of VertigoPrehospital IdentificationConclusionReferencesSyncope and vertigo are often used interchangeably. This is not accurate, although both are forms of vertigo. The term 'Dizziness' is given when a patient experiences changes in consciousness, movement, sensation and perception. The term "Dizziness" can be divided into four different types; Psychologically induced syncope/presyncope, imbalance, vertigo and 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). Say no to plagiarism. Get a tailor-made essay on "Why Violent Video Games Shouldn't Be Banned"? Get an Original Essay Syncope and Presyncope Cardiac irregularities and cerebral hypoperfusion are known to be directly related to syncope and presyncope. Presyncope is the medical term that describes both the sensation of impending fainting and/or lightheadedness, preceding an episode of syncope. It is the actual loss of consciousness that is transitory in nature. Based on the Sharpey-Schafer model, “syncope is the result of acute systematic vasodilation potentially triggered by the forced contraction of an empty left ventricle” (Sharpey-Schafer, 1956). Syncope can be divided into neurally mediated syncope (NMS) and cardiac syncope/heart rhythm disorders (Saccomano, 2012). Pathophysiology of Neuromediated Syncope Neuromediated syncope (NMS), also known as reflex or vagal syncope, is the most common cause of syncope. in otherwise healthy patients, particularly young women (Fu & Levine, 2014). NMS is the sudden transient loss of consciousness resulting from an intense and sudden decrease in blood pressure, often following changes in posture and cerebral hypoperfusion, and is known for its spontaneous recovery (Puppala, Dickinson, & 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 through cardiovascular reflexes and maintained within adequate margins (cardiovascular homeostasis). If these are altered, neurocardiovascular reflex mechanisms come into play. When we stand, blood pools towards our extremities. In a few minutes, more than half a liter of blood remains trapped in the veins located under the heart, while the circulating plasma moves 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 transmitted to the central nervous system once detected by the baroreceptors. . Once 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 studies have suggested that regardless of the strong reduction in blood pressure, the prerequisite for the suspension of sympathetic activity is no longer accurate (Malamud-Kessler et al., 2016), however research needs to be conductedmore in-depth. 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 elevated 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 that reduce circulating blood volume and cardiac output, resulting in a syncopal event (Saccomano, 2012). Several heart disorders are associated with the two main symptoms of syncope, lightheadedness and acute loss of consciousness, and they are as follows; sick sinus syndrome, heart block, mitral valve prolapse and aortic stenosis (Saccomano, 2012). Clinical presentation of syncope Neuromediated syncope – characterized by prodromal symptoms approximately 1 minute before syncope and includes; nausea, diaphoresis, abdominal discomfort, pallor, diaphoresis, yawning and hypotension (Malamud-Kessler et al., 2016). These symptoms are typically followed by difficulty concentrating, headache or 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 have recurrent presyncopal episodes. Episodes often occur when patients change positions rapidly, from sitting to standing, or have been standing for prolonged periods of time. These patients do not present ECG changes (Malamud-Kessler et al., 2016). Cardiac syncope – characterized by prodromal symptoms similar to those of NMS, but with reduced prevalence of lightheadedness, hypotension, and other preceding symptoms. ECG changes are common, and these patients are at significant risk for cardiac arrest (Tretter & Kavey, 2013). Based on Tretter & Kavey's 2013 study, all patients who suffered cardiac syncope had both; “(1) history of syncope associated with exertion; (2) a cardiac-related family history; (3) an abnormal physical exam; or (4) an ECG interpreted as abnormal by a pediatric cardiologist” (Tretter & Kavey, 2013). Vertigo Vertigo includes sensations related to changes in the environment or in oneself. It is often described as; rotations, tilts, back and forth movements, rotations and sensations of imbalance, which are often exacerbated by actual movement. Vertigo is primarily related to both the central nervous system (uncommon) and the peripheral nervous system (common) (Saccomano, 2012). Pathophysiology of central vertigo The vestibular system 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 inside the inner ear and is made up of three canals; utricle, saccule and semicircular. Neuroepithelial hair cells are found within these channels. These hair cells send projections across the vestibulocochlear nerve division 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 result from a localized dysfunction or lesion on any of these vestibular structures. In these cases, the patient experiences a "hallucinatory movementenvironment” and/or spins, resulting in dizziness (Tadi., 2019; Thompson & Amedee, 2009). Underlying medical disorders 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 cerebellar or posteroinferior vertebral arteries, resulting in acute lateral medullary syndrome, is the most commonly known underlying cause of central vertigo. Thompson & Amedee, 2009). Rare cause of central vertigo is drug toxicity, particularly in common anticonvulsant drugs (Tadi., 2019). medium, compromise the vestibular pathway system. The labyrinth system is responsible for both balance and eye movements. When this pathway is altered, it generates an impairment of cortical integration and an overload of the pathway, resulting in misinterpretation of sensory data. received (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's disease (Saccomano, 2012; Taylor., 2019; Thompson & Amedee, 2009 ). Clinical presentation of Central Vertigo – characterized by gradual onset vertigo, spinning sensation, rotational environment, nystagmus, brainstem signs and symptoms, and a history of migraines, tumors, or multiple sclerosis (Tadi., 2019; Thompson & Amedee, 2009) . Peripheral – characterized by abrupt onset of tinnitus, hearing disturbances, predominant vestibulocochlear signs, difficulty concentrating, nausea or vomiting (Taylor., 2019; Thompson & Amedee, 2009). Prehospital Identification When caring for a patient with dizziness it is imperative to first rule out other factors, such as; drugs, alcohol, stroke, anxiety, seizures or medication use (Tadi., 2019). Once these are ruled out, the next step would be; take a complete and thorough medical history; from head to toe; 12-lead ECG acquisition; Blood pressure monitoring; focused neurological examination, including Babinski's sign; targeted cardiovascular examination; and an accurate account of signs/symptoms and their frequency, where possible. To exclude BPPV, the paramedic, if trained to do so, may be able to use the Dix-Hallpike maneuver in case of contraindications; cervical instability; carotid sinus syncope; vertebrobasilar insufficiency; other vascular disorders are not present. If symptoms occur, BPPV is likely the cause (Tadi., 2019; Walther, 2017). In suspected BPPV, stroke can be excluded if the HiNTs examination is negative (Tadi., 2019; Walther, 2017). . The HiNTs exam is a three-part, in-depth and extensive occulomotor neurological evaluation used by medical professionals to rule out a stroke or identify the location of the lesion. For this evaluation to be indicated, the patient must have at least one risk factor for stroke. However, paramedics would require additional training to utilize and understand this assessment and outcome (Kattah, Talkad, Wang, Hsieh, & Newman-Toker, 2009; Tadi., 2019). When taking your medical history, be sure to inquire about any past or current inner ear and labyrinth disorders, as well as a history of migraines or tumors, as they suggest that the likely diagnosis is dizziness. While, if the patient claims to000141