SYNCOPE WITH UNCERTAIN ETIOLOGY
A – The patient’s underlying disease process
The patient is an 89-year old white male whose past medical history includes non-insulin dependent diabetes mellitus, anemia, gastroesophageal reflux disease, dementia, possible bone cancer, and chronic obstructive pulmonary disease. He was brought to the hospital because he fainted while eating breakfast. His past surgical history is not known. He is a widower with two children and currently a retired fireman. Thirty five years ago, he quit smoking but still drinks two to three beers per week presently.
A review of systems showed no complaints from the patient with regards to cardiovascular, pulmonary, gastrointestinal, genitourinary, musculoskeletal, dermatologic, and changes in the senses. However, the patient admits that he did have an episode of passing out or syncope. The patient is also positive for dementia and depression.
Physical examination revealed that the patient’s own subjective feelings are in line with the results. There are no abnormalities found in the patient’s systems. His laboratory results showed Sodium 131, Potassium 4.0, Chloride 96, Carbon Dioxide 31, Blood urea nitrogen 15, Creatinine 0.9, Glucose 241, Calcium 8.5, White blood cell count 1.6, Hemoglobin 1.6, Hematocrit 32.7, and Platelets 45. All the other values from the laboratory tests show normal values except for Sodium which is slightly decreased from the normal 136-145 meq/L, Carbon dioxide content increased from the normal 24-29 meq/L, Hemoglobin slightly decreased from the normal 2.09-2.79mmol.L, Hematocrit decreased from the normal 40-52%, and the Glucose count significantly elevated from the normal 65-110 mg/dL values. Most importantly, the patient showed signs of bradycardia or slow heart rate as seen on his vital signs pulse 66, respirations 16, and blood pressure 162/66.
B – Expected disease course/prognosis
Syncope was defined as a sudden transient loss of consciousness associated with an inability to maintain postural tone that was not compatible with vertigo, seizure, dizziness, shock, coma, or other states of altered consciousness (1990). Syncope occurs on sudden onset, often associated with emotional crisis or heart block. The coma is seldom deep and prolonged, with pallor. The pulse is slow at onset and later rapid and weak. Fainting, or syncope, is sudden, transient loss of consciousness. It can be due to metabolic or neurologic abnormalities, but more commonly it is due to peripheral vascular or cardiac abnormalities that cause inadequate cerebral blood flow. It is often benign and it is most commonly due to abrupt vasodilation. This produces hypotension, generally in association with bradycardia (2000).
C – Symptoms and signs typically manifested
Syncope has a broad differential diagnosis. Syncope can also be due to more serious abnormalities, which is probably the case for this patient. About 25% of syncope are of cardiac origin and are due to either transient obstruction of blood flow through the heart or sudden decreases in cardiac output owing to various cardiac arrhythmias. Fainting due to bradycardia, heart block, or sinus arrest is called neurocardiogenic syncope. In addition, fainting is the presenting symptom in 7% of patients with myocardial infarctions. Thus, all cases of syncope should be investigated to determine the cost (2001).
Differential diagnoses of the patient include cardiovascular etiology with bradycardia versus neurologic disturbance versus blood sugar abnormality which is very much visible in his glucose level results. Bradycardia is most frequently the result of increased vagal tone. The condition is a result of slowed diastolic depolarization within all the S-A pacemaker cells.
The patient is also shown to be positive for orthostatic hypotension 125/72 while lying down, 121/46 while sitting up, and 76/46 while standing. Orthostatic hypotension is defined as a drop in blood pressure of at least 20 mm Hg systolic or 10 mm Hg diastolic within three minutes of standing. Tachycardia and a heart rate greater than 100 beats per minute during testing indicate volume depletion. Minimal cardiac acceleration suggests baroreflex impairment that may occur normally in older patients. Medications associated with orthostatic hypotension include antihypertensives, antidepressants, and diuretic agents. Autonomic insufficiency secondary to diabetes mellitus or alcohol abuse also may cause orthostasis (2005).
D – Etiology
The term vasovagal syncope has been coined to denote this entity (2001). Postural syncope is fainting due to pooling of blood in the dependent parts of the body upon standing. Micturition syncope, fainting during urination, occurs in patients with orthostatic hypotension. It is due to the combination of the orthostasis and reflex bradycardia induced by voiding in these patients. Pressure on the carotid sinus, produced, for example, by a tight collar, can cause such marked bradycardia and vasodilation that fainting results (carotid sinus syncope). Rarely, vasodilation and bradycardia may be precipitated by swallowing (deglutition syncope). Cough syncope occurs when the increase in intrathoracic pressure during straining or coughing is sufficient to block venous return. Effort syncope is fainting on exertion as a result of inability to increase cardiac output to meet the increased demands of the tissues and is particularly common in patients with aortic or pulmonary stenosis ( 2001).
Within the cardiology context, a stimulation which can cause a reflex drop in heart rate and blood pressure can cause syncope and is normally a problem for older adults (2004).
E – Related factors
Heart conditions as well as diabetes mellitus could be hereditary and play a role in a patient’s syncope episodes. Drugs are also a relatively common cause of syncope, especially in elderly patients. Older persons often take multiple medications, and the addition of sedatives, decongestants or anti-diarrheal medications can result in tachyarrhythmias and cognitive changes. Some ophthalmologic medications can aggravate bradyarrhythmias or heart block (1995). Additionally, activities that involve stretching the neck, such as shaving or looking back over one’s shoulder, can produce carotid sinus syncope. The relationship of syncope to meals or alcohol or drug ingestion is also important.
F – Expected medical surgical and nursing treatment.
Treating syncope is empiric given the fact that generally, specific physiologic triggers of syncope are not identified. Infrequent episodes of syncope require only observation and counseling. When it comes to nutrition, there may be a need to increase in hydration and sodium or salt intake, especially in warm weather. Treatment options using pharmacologicals include anticholinergic agents, selective serotonin reuptake inhibitors, beta-adrenergic blockers, adenosine receptor blockers, mineralocorticoids and anticonvulsants. It is also recommended to use compression hose and pacemakers (2001). Details of treatment follow.
The differential diagnoses include cardiovascular etiology with bradycardia versus neurologic disturbance versus blood sugar abnormality which is very much visible in his glucose level results. This is neurocardiogenic syncope which is fainting due to bradycardia, heart block, or sinus arrest. Further evaluation and treatment with regards to cardiology will be continued. As for the elevated glucose levels, due to his diabetes, the patient will have to continue taking Glipizide and Accu-Checks. As with regards to the decreased Sodium levels or hyponatremia, it will be monitored and a fluid restriction of less than 1,000 cc’s per day will be done.
The patient’s Protonix 40 will be continued for his gastroesphageal reflux disease. All other medicines like Aricept for dementia and Lexapro for depression will be continued. Oxygen for chronic obstructive pulmonary disease will be used as needed. The patient will be continually evaluated and monitored.
G – Pertinent nutritional data; address the patient’s nutritional status as it relates to the patients disease process
Glucose control and lots of fluid intake should be included in the diet of the patient. Fluid and salt replacement may be accomplished by mouth or through intravenous therapy.
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