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Sweet 1 Christina Sweet PTP 546 June 11, 2012 Paper 2: Patient Interview Treatment of Neurocardiogenic Syncope Introduction Patient is a 22 year old Caucasian male. He is a non-smoker, highly active, and athletic. He is 6 foot 2 inches and 195 pounds; patient reports having lost 45 pounds in the last 9 months through dieting, working out, and discontinuing use of a glucocorticoid. He has a self-reported history of sustaining multiple concussions from playing football in high school, as well as obtaining various musculoskeletal injuries from playing competitive sports. Patient also reports getting severely “beat-up” while in high school that resulted in hospitalization and continues to cause him TMJ problems that have been linked to reoccurring headaches. He has a family history of cancer, heart failure, and sleep apnea on his father side and on his mother’s side patient reports history of stroke as well as both his mother and uncle commonly passing out for an unidentifiable cause. Patient also has a left testicle Varicocele that developed at age 13, but has not shown signs of growth. Patient reports having had no surgeries. Medical Diagnoses Patient reports that at age 15 he started passing out. The first incident occurred while the patient was riding his bike; he says he felt dizzy and nausea, and collapsed upon getting off his bike. The second incident occurred while patient was at a football practice after sprinting on a hot day; he says he remembers feeling light-headed and then the next thing he was waking up on the grass. After the second time passing out, he had a tilt-table test performed. He passed out on the table 5 minutes into the test and was therefore suspected to have a syncope. Syncope is Sweet 2 known for being a sign of heart value or arrhythmia problems.1 Patient reports having an esophageal echo to look at the backside of his heart to identify if there was a hole between the left and right ventricle. The echo found no hole in the heart so a surgical solution was ruled out. Without a structural defect of the heart being identifiable the patient was diagnosed with Neurocardiogenic syncope also known as neurally mediated hypotension or vasovagal attack. Neurocardiogenic syncope is a “benign non- cardiac cause of fainting in athletes” that is caused by a disorder of the autonomic system responsible for regulating the cardiovascular system.1 Activities such as prolonged standing after exertion, a warm environment, or stress occurring during exercises usually precipitate a person’s fainting with this disorder. Neurocardiogenic syncope’s etiology is still debated, but it is believed to be a mechanoreceptor problem on the ventricles that registers a person’s blood pressure to be higher than it actually is. This leads to the incorrect sympathetic and parasympathetic activity occurring that is needed for physical exertion. The autonomic system slows the heart and dilates blood vessels, which is the opposite effect that is needed to maintain consciousness while exercising. This is a non-life threatening disorder; however the signs of fainting should be monitored when working with this patient. Pharmacological Treatment The patient was prescribed an anti-hypotensive drug from age 16 to 20 to keep his blood pressure up so he would not pass out, but does not remember the name of it. Patient reports that he went off the anti-hypotensive drug because he felt he did not need it anymore, but that upon discontinuing use of the drug his blood pressure remained high. He was given a glucocorticoid, named fludrocortisone to help regulate his blood pressure. The patient took fludrocortisone for about a year, but stopped usage for the undesirable weight gain it caused. Currently the patient is not taking any medication for his condition; however he notes that he has recently been Sweet 3 experiencing syncope symptoms like light-headedness, malaise, and headaches when he performs strenuous work. Therefore it may be suggested that the patient is experiencing reoccurring Neurocardiogenic syncope that is characterized by exercise induced hypotension and bradycardia. Education on how to monitor his blood pressure is needed, along with explaining the need for continued use of an anti-hypotension drug that effects the autonomic system like an adrenergic drug. Patient Knowledge When discussing Neurocardiogenic syncope and treatment with a medication the patient seems to be knowledgeable about the symptoms of the condition and understands the need to raise his blood pressure. The patient reports that he hates the feeling that he is about to faint and therefore seems eager to get it managed. The patient is aware that his condition involves an improperly working heart, however is unaware of the autonomic pathophysiology of his disorder and he believes that he just has a cardiac problem of hypotension. He does not recognize that his blood pressure is normal at rest (118/75 mmHg) and that only when he exerts himself does his sympathetic cardiac system fail to properly regulate his blood pressure. The patient admits that the blood pressure numbers confuse him and that he just goes by if the nurse or doctor says it is good or bad. Since the patient took a hypertensive drug for 4 years for this condition he is familiar with the administration and side effects of the drug, he reports taking the drug once a day orally in the morning with food. He reports his side-effects were weight gain and decreased sex drive. The patient also understands that if he feels symptoms of syncope that he is supposed to sit or lay down and eat and drink lots of fluids. Like it was mention before the patient does not understand blood pressure measurements and therefore he leaves this condition to be monitored at his check-ups. Sweet 4 Pharmacological Information The patient does not remember the specific anti-hypotensive he was on 2 years ago, however as an adrenergic drug is needed it may be predicted that he was on a drug like Midodrine, an alpha-1 agonist that causes vasoconstriction and thus is an anti-hypotensive. Its trade names are Amatine, ProAmatine, and Gutron, which all act by activating the alpha-1 adrenergic receptors that causes an increase in vascular tone and consequently raises blood pressure.2 Midodrine is a fast acting drug with a peak effect occurring about half an hour after taking it. Peak blood concentrations occur about 1 to 2 hours after a dose and it has a half-life of about 3 to 4 hours.3 Dosage of Midodrine comes in 2.5-mg, 5-mg and 10-mg tablets, with a typical dosage depending on patients resting blood-pressure.2 A typical adult dosage is 10-mg three times a day in approximately 4-hour intervals during daytime hours.4 Reported mild side- effects of Midodrine are headache, feeling of pressure and fullness in the head, dry mouth, nervousness, anxiety, and rash. The occasional serious side effects of Midodrine are chest pains, fluttering heart beats and an excessive increase in blood pressure when lying down, which if accompanied with increased awareness of a heartbeat, pounding in the ears, headache and blurred vision should be reported to a doctor or emergency treatment. It is suggested that a patient does not take Midodrine 3-4 hours before bed or anytime they are going to be laying down for an extended period of time.2 Additionally confusion and thinking abnormally had been reported and could be potential dangerous if it lead to self-injury. In recent years there have been FDA proposals to remove Midodrine, however it still remains on the market as an anti- hypotensive.5 Other studies on treatment of Neurocardiogenic syncope have proposed beta- blockers as a form of treatment for its effects on decreasing the activity of the sympathetic nervous system.6 Sweet 5 Impact on Physical Therapy From a physical therapy perspective if we were evaluating this patient and discovered that he had signs and symptoms of syncope that had not been treated, this would count as a red flag and mandate that we make a medical referral to have it checked out by a physician/ cardiologist. Heart issues like syncope can be life-threatening, especially in the presence of risk factors for stroke or heart attack and therefore it is always safest to have an all-clear before proceeding with treatment. However if this patient came to us already diagnosed with Neurocardiogenic syncope and was controlling it with medications then we would want to make sure he had taken his medication recently, optimally within the last hour so that we are in the peak effect window of half hour to hour to decrease the risk of him having an adverse cardiac event during treatment We would want to closely monitor his blood pressure before and during exercise to make sure he was not having hypotension with exertion. At the same time we need to make sure that the dosage is appropriate, and that the patient is not having tachycardia or extreme hypertension. Even though his is an athletic young man we would still want to initially keep the intensity lower than the threshold at which his symptoms would appear to be able to judge his tolerance and give us a baseline to progress him safely from. As for monitoring the side effects of the drug as PT’s we would be most concerned with the excessive hypertension and the confusion, as the hypertension could lead to a cardiac event and the confusion could lead to injury in and outside the clinic for the individual. Conclusion In conclusion understanding the physiology behind Neurocardiogenic syncope and how it can be regulated with an adrenergic drug will help us to treat patients with this disorder safely Sweet 6 and decrease the chance of adverse cardiac events happening during treatment. Furthermore we can help patients determine the exertion threshold for their hypotension and syncope symptoms to occur. For this patient specifically that is athletic and wants to participate in sports, we could help him determine what is the optimal time for him to take his anti-hypotension medication so that he can have the best control of his blood pressure during competition. Furthermore we can help him figure how hard he can push himself and educate him how to hydrostatically control his hypotension in the case that his medication is not effective or available. References 1 rd Goodman, C. C., Fuller, K. S. Pathology: Implications for the Physical Therapist. 3 ed. 2009; 522-523. 2 Silberstein, S. D., Marmura, M. J., Muntne, N. Essential Neuropharmacology: The Prescriber's Guide. 2008. 3 Wright, R.A, Kaufmann, H.C., Perera, R., et al. A double-blind, dose-response study of midodrine in neurogenic orthostatic hypotension. Neurology. Jul. 1998;51(1):120-4. 4 Mayo Clinic. Drugs and Routes: Midodrine. Mayo Foundation for Medical Education and Researc.h Nov. 11, 2011 <http://www.mayoclinic.com/health/drug-information/DR600931/DSECTION=proper-use>. 5 O'Riordan, M . "FDA recommends withdrawal of midodrine". Food and Drug Administration. FDA proposes withdrawal of low blood pressure drug [press release]. Aug. 16, 2010. 6 Chen-Scarabelli, C., Scarabelli, T.M. Neurocardiogenic syncope. British Medical Journal. Aug. 7, 2004; 329(7461): 336–341.
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