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Neurocardiogenic Syncope (NCS) (also known as vasovagal syncope orneutrally mediated syncope) can, in a layman’s language, bedescribed as fainting, blackout or passing out. Temporary loss ofconsciousness is caused by a rapid drop in blood pressure followed byvery fast heart rate. The heart rate then slows down below the normallevel resulting to the inconsistent flow of blood and oxygen to thebrain. NCS is a common outpatient case accounting for 3% of allemergency cases and 6% of the total number of admissions tohospitals. Ideally, it occurs in all age groups but more prevalent inadvanced age than in the young age. For instance, 15% of the casesoccur in children under the age of 18 while 23% occur in seniorcitizens with the age of 70 years and above. The probability that theattack reoccurs is 30%. One of the essential factors when treatingNCS is distinguishing it from other causes of fainting.

In most cases, NCS occurs when a person is standing as oppose to whenthey are sitting or sleeping (Johnston et al., 2016, page1385). This is because standing makes blood move to the lowerextremes which result to lower supply of blood in the upper parts ofthe body including both the heart and the brain. In its adjustment tothe lower blood supply in the upper organs, the body increases thevascular tone, the rate of heart beat and the cardiac output. Theblood vessels contract to ensure that the normal rate of bloodpressure is maintained. The normalcy may, however, not be maintaineddepending on the health condition of the individual and, instead,drops slightly from the normal. This is the mechanic operation of thebody of a healthy human being who does not experience NCS. Anyalteration from the normal operation leads to loss of consciousness(McGrady et al., 2013, page 261).

As pointed out earlier, NCS commences with a sudden drop in bloodpressure that causes the heart to make harder and faster contractionsin an attempt to compensate the sudden drop. This creates asimulation to receptors in the heart to send a message to the brainthrough the nerves that the heart is pumping harder and faster thanthe normal rate (Dick, 2015, page 339). The cardiovascular center,specifically its sympathetic portion, is stimulated to reduce itsimpulse to the heart and blood vessels to correct the situation. Thevagal nerve, on the other hand, increases its impulses. As a resultof these reflexes of the nervous system, the heart slows down and insome cases, it stops. The system’s reflex also causes the bloodvessels to open up in an attempt to reduce the blood pressure(In-Caplan, 2014, page 179). The simultaneous occurrence of thesereflex actions causes the inadequate flow of blood to the brain whichleads to fainting.

The causes of NCS are not limited to the mechanism described above.There are several other conditions that cause NCS, and they maycomplicate physician’s attempts to diagnose for the loss ofconsciousness. In fact, the majority of physicians point out thatdetermining the cause of loss of consciousness for a patient duringthe first time is the most challenging activity. For one to concludethat a patient is suffering from NCS, a clear description of thesymptoms, frequency, and pattern of triggers by the patient isparamount (In-Caplan, 2014, page 182). The challenge is that mostpatients do not clearly understand what transpires before theirunconsciousness. For those who do so, they have difficultiesexplaining it. In many of the cases, therefore, medics findthemselves treating the wrong cause of NCS. To improve the diagnosticaccuracy of tests on NCS patients with recurrent attacks, tests suchas the tilt table, event monitor, echocardiogram, electrophysiologyand implanting a loop recorder can be used. Even so, irrespective ofthe trigger or the cause, the mechanism remains as describe above.Effective treatment is, however, not based on the mechanism but thetrigger or the cause (Johnston et al., 2016, page 1385). Thiscreates the difference. However, as it will be well evident later inthis discussion, NCS treatment is mainly based on physical activitiesand exercises as opposed to medications and pacemakers.

At the onset of NCS (before complete unconsciousness), patientssuffer from the initial consequences of the condition which can alsobe described as the initial symptoms. The main consequence islightheadedness where some of the patients feel that they cannot feeltheir head (Burns, 2013, page 706). Some patients feel dizzy, weakand experience fever. The condition may as well lead to fatigue,nausea, and abdominal pains even without any physical abdominalinjury. Confusion, sweating, and visual disturbances are also majorconsequences. The consequences differ from one individual to theother, but all of them are related to the operations of theindividual’s nerves and the fact that the brain and the heart lacksufficient supply of blood and oxygen. In all cases, though, a fasterthan normal heart rate is inevitable. In fact, the high rate of heartbeat is the main cause of other consequences and the main trigger ofactual fainting.

After regaining their consciousness, the majority of the patientsvomit or experience nausea. Nausea with successive vomiting may aswell occur before losing consciousness. Vomiting, visual and verbaldifficulties are also common consequences of NCS, especially forpresyncope patients. These are patients who suffer from the attackwith partial loss of consciousness as opposed to entire loss. Incases where individuals lose their consciousness while sittingwithout passing out, the main consequence is pale or gray look.Moreover, they may start yawning and acquire a blue, purple or redcoloring. As at that time, they are already suffering from NCS andwhat follows is passing out. In addition to these consequences,patients also feel unwell after regaining their consciousness (Van etal., 2013, page 464). The majority are said to complain of aheadache and malaise. NCS also leads to repeated pass outs. Theattack also places the life of the patient at high risk of danger offalling on dangerous grounds that may cause physical injuries.

The best was to avoid NCS is preventing it rather than curing. Themain preventive strategies include increasing salt consumption, food,fluids and total avoidance of meal skipping (Swaiman, 2012, page908). Besides, taking cool showers is a major precautionary measure.Besides, although most physicians will advise, individuals shouldform a habit of laying down during blood tests and vaccines. When onefeels the symptoms of NCS, it is advised that they should lay downquickly. Alternatively, one is also advised to sit down with the headbetween the knees so that the flow of blood to the brain can beincreased.

Medics rarely use medications and pacemakers to treat the condition.In most cases, NCS’s treatment is based on avoidance of triggers,restoration of brain blood flow and prevention of pathophysiologicmechanism (Rowland et al., 2011, page 1068). NCS treatment is,therefore, based on the specific triggers in an individual. Forinstance, if the trigger is the sight of blood, the best treatment isexposure based exercises. On the other hand, if the trigger is aspecific drug, then its avoidance is the only treatment. As such, NCStriggered by a specific drug cannot be treated with exposure basedexercises. The treatment should be consistent with the cause. Aspointed out earlier, it is challenging for physicians to identify thecause of loss of consciousness especially for first time patients.Consequently, treatment becomes difficult.

To sum up, there are several biological activities that occur in thebody of an NCS patient before, during and after the attack. The maincause of NCS as well evident in the mechanism is a rapid drop inblood pressure followed by very fast heart rate which then slowsdown. The attack occurs more prevalently when one is standing thanwhen they are seated. The main consequences include reoccurrence (theprobability after the first occurrence is 30%), fatigue, nausea,abdominal pains, confusion, headache and pale or gray look (Noggle etal., page 270). Prevention is a better treatment for NCS thancuring. NCS patients are advised to increase their rate of saltconsumption, food, and fluids. Physicians recommend that the triggeris identified before treatment to avoid providing the wrongprescription since the attack’s treatment relies on the cause.

WorkCited

Burns, Catherine E. Pediatric Primary Care. Philadelphia, PA:Saunders Elsevier, 2013. Internet resource.

Caplan, Gideon. Geriatric Medicine: An Introduction.Melbourne, IP Communications, 2014. Print.

Dick, Macdonald. Clinical Cardiac Electrophysiology in the Young., 2015. Internet resource.

Johnston, Michael V, Harold P. Adams, and Ali Fatemi. Neurobiologyof Disease. New York, NY: Oxford University Press, 2016. Print.

Kusumoto, Fred, and Nora Goldschlager. Cardiac Pacing for theClinician. New York: Springer, 2008. Internet resource.

McGrady, Angele, and Donald Moss. Pathways to Illness, Pathways toHealth. New York, NY: Springer, 2013. Internet resource.

Noggle, Chad A, Raymond S. Dean, and Arthur M. N. Horton. TheEncyclopedia of Neuropsychological Disorders. New York: SpringerPublishing Co, 2012. Print.

Rowland, Lewis P, Timothy A. Pedley, and H H. Merritt. Merritt`sNeurology. Philadelphia, PA: Lippincott Williams &amp Wilkins,2011. Print.

Swaiman, Kenneth F. Swaiman`s Pediatric Neurology: Principles andPractice. Edinburgh: Elsevier Saunders, 2012. Internet resource.

Van, Huffel S, Gunnar Naulaers, Alexander Caicedo, Duane F. Bruley,and D K. Harrison. Oxygen Transport to Tissue Xxxv. New York:Springer, 2013. Print.