Wednesday, May 7, 2008

Case Presentation on Syncope

Sponsored links

Case Summmary:
This is a case of a 24-year-old man brought to the emergency department (ED) after several episodes of nearly blacking out. He also experienced palpitations with associated light-headedness. An electrocardiogram (ECG) is obtained, and a diagnosis of Syncope was considered. Proper Interventions were then given to prevent complications of the disease condition.

Chief Complaint:
Episodes of nearly blacking out, light-headedness, and palpitations.

History of Illness:
A 24-year-old man presents to the emergency department (ED) after several episodes of nearly blacking out that have occurred 3-4 times over the past 3 days. The patient states that he also felt his “heart beating really fast” and associated light-headedness. He smokes 2-4 packs of cigarettes per day and has done so for 5-6 years. No history of significant cardiac disease or sudden cardiac death in his family is noted.

II.Case Discussion

What is syncope?
Syncope (SIN'ko-pe) is temporary loss of consciousness and posture, described as "fainting" or "passing out." It's usually related to temporary insufficient blood flow to the brain.
It most often occurs when the blood pressure is too low (hypotension) and the heart doesn't pump a normal supply of oxygen to the brain.

Syncope occurs when cerebral perfusion globally decreases. Brain parenchyma depends on adequate blood flow to provide a constant supply of glucose, the primary metabolic substrate. Brain tissue cannot store energy in the form of high-energy phosphates found elsewhere in the body; therefore, a cessation of cerebral perfusion lasting only 3-5 seconds results in syncope. Cerebral perfusion is maintained relatively constant by an intricate and complex feedback system involving cardiac output, systemic vascular resistance, arterial pressure, cerebrovascular resistance with intrinsic autoregulation, and metabolic regulation. A clinically significant defect in any one of these or subclinical defects in several of these systems may cause syncope.
Any of the following may manifest as syncope. Cardiac output can be diminished secondary to mechanical outflow obstruction, pump failure, hemodynamically significant arrhythmias, or conduction defects. Systemic vascular resistance can drop secondary to vasomotor instability, autonomic failure, or vasodepressor/vasovagal response. Arterial pressure decreases with all causes of hypovolemia. A central nervous system (CNS) event, such as a hemorrhage or a seizure, can also present as syncope. Syncope can occur without reduction in cerebral blood flow in patients who have severe metabolic derangements (eg, hypoglycemia, hyponatremia, hypoxemia).

What causes syncope?
It may be caused by emotional stress, pain, pooling of blood in the legs due to sudden changes in body position, overheating, dehydration, heavy sweating or exhaustion. Syncope may occur during violent coughing spells (especially in men) because of rapid changes in blood pressure. It also may result from several heart, neurologic, psychiatric, metabolic and lung disorders. And it may be a side effect of some medicines.
Some forms of syncope suggest a serious disorder:
• those occurring with exercise
• those associated with palpitations or irregularities of the heart
• those associated with family history of recurrent syncope or sudden death

Management of Syncope
The majority of children and young adults with syncope have no structural heart disease or significant arrhythmia (abnormal heart rhythm). So, extensive medical work-up is rarely needed. A careful physical examination by a physician, including blood pressure and heart rate measured lying and standing, is generally the only evaluation required.
In other cases an electrocardiogram (EKG or ECG) is used to test for abnormal heart rhythms such as long Q-T syndrome. This is a genetic heart condition that can cause sudden cardiac death. Other tests, such as exercise stress test, Holter monitor, echocardiogram, etc. may be needed to rule out other cardiac causes of syncope.
If EKG and cardiac tests are normal, the person will undergo a tilt test. The blood pressure and heart rate will be measured while lying down on a board and after the board is tilted up. Someone who has NMS will usually faint during the tilt, due to the rapid drop in blood pressure and heart rate. As soon as the person is placed on his or her back again, blood flow and consciousness are restored.
To help prevent syncope, people with NMS should be on a high-salt diet and drink plenty of fluids to avoid dehydration and maintain blood volume. They should watch for the warning signs of fainting — dizziness, nausea and sweaty palms — and sit or lie down if they feel the warning signs. Some people also may need medication.
Prehospital Care
Prehospital management of syncope covers a wide spectrum of acute care and includes rapid assessment of airway, breathing, circulation, and neurologic status.
• Treatment may require the following:
• Intravenous access
• Oxygen administration
• Advanced airway techniques
• Glucose administration
• Pharmacologic circulatory support
• Pharmacologic or mechanical restraints
• Defibrillation or temporary pacing
• Advanced triage decisions, such as direct transport to multispecialty tertiary care centers, may be required in select cases.
Emergency Department Care
In patients brought to the ED with a presumptive diagnosis of syncope, appropriate initial interventions include intravenous access, oxygen administration, and cardiac monitoring. ECG and rapid blood glucose evaluation should be performed promptly. Syncope may be the manifestation of an acute life-threatening process but is generally not emergent. Clinically ruling out certain processes is important. The treatment choice for syncope is dependent upon the cause or precipitant of the syncope. Patients in whom a cause cannot be ascertained in the ED, especially if they have experienced significant trauma, warrant supportive care and monitoring.
• Situational syncope treatment focuses on educating patients about the condition. For example, in carotid sinus syncope, patients should be instructed not to wear tight collars, to use a razor rather than electric shaver, and to maintain good hydration status; they should also be informed of the possibility of pacemaker placement in the future.
• Orthostatic syncope treatment also focuses on educating the patient. Inform patients about avoiding postprandial dips in BP, teach them to elevate the head of their bed to prevent rapid BP fluctuations on arising from bed, and emphasize the importance of assuming an upright posture slowly. Additional therapy may include thromboembolic disease (TED) stockings, mineralocorticoids (eg, fludrocortisone for volume expansion), and other drugs such as midodrine (an alpha1-agonist with vasopressor activity). Patients' medications must be reviewed carefully to eliminate drugs associated with hypotension. Intentional oral fluid consumption is useful in decreasing frequency and severity of symptoms in these patients.
• Cardiac arrhythmic syncope is treated with antiarrhythmic drugs or pacemaker placement. Consider cardiologist evaluation or inpatient management since this is more commonly associated with poor outcomes. Trials assessing beta blockade to prevent syncope have conflicting results, but no clear effect has been demonstrated.
• Cardiac mechanical syncope may be treated with beta-blockade to decrease outflow obstruction and myocardial workload. Valvular disease may require surgical correction. This, too, is associated with increased future morbidity and mortality.
• Neurologic syncope may be treated in the same fashion as orthostatic syncope, or it may be treated with antiplatelet medications. Patients are recommended to have neurologic follow-up care to determine whether they need further neurovascular imaging.

Drug Category: Anticholinergics
These agents improve conduction through the AV node by reducing vagal tone via muscarinic receptor blockade. For patients with infranodal block, this therapy is ineffective.
Drug Category: Nutrient supplements
Parenterally injected dextrose is used in patients unable to sustain adequate oral intake. Its direct oral absorption results in a rapid increase in blood glucose concentrations.
Drug Category: Benzodiazepines
CNS agents of the 1,4-benzodiazepine class exert their effects by binding at stereo-specific receptors in the CNS. Their exact mechanism of action has not been clearly elucidated. Benzodiazepines cause a dose-related CNS depression, which varies from mild sedation to hypnosis.
Drug Category: Vasopressor
Midodrine forms an active metabolite, desglymidodrine, that is an alpha1-agonist acting upon receptors of the arteriolar and venous vasculature.

• Education may have a substantial impact on the prevention of recurrence, especially in situational and orthostatic syncope. Patients may be trained to avoid situations that prompt syncope in situational cases. In orthostatic syncope, patients should drink 500 mL of fluid each morning in addition to their usual routine and should avoid standing up too quickly.

III. Conclusion
The thorough history of the patient with syncope should begin with the observations of onlookers.
The history also should include the identification of aggravating and alleviating factors, especially the additions of new medications. Antiarrhythmic and antihypertensive medications raise the possibility of proarrhythmia or orthostasis. Phenothiazines and tricyclic medications predispose older patients to orthostasis. Over-the-counter medications and supplements also can contribute to syncope.
The physical examination of a patient with syncope should include measurements of blood pressure and pulse rate in the upper and lower extremities while the patient is in the supine and upright positions to identify orthostatic hypotension, autonomic dysfunction, or possible organic heart disease. Checking for carotid bruits can find impaired cerebral blood flow or underlying coronary artery disease. On examination, the physician also may find signs of pulmonary hypertension, left ventricular dysfunction, valvular heart disease, or other forms of organic heart disease. Neurologic disorder is suggested by abnormal cognition, speech, visual field, motor strength, sensation, tremor, or gait disturbance.
Syncope is not associated with increased mortality when no underlying heart disease is present. When the initial evaluation is normal, it is often challenging to discern the origin of syncope. Although many of the most serious possible causes of syncope can be excluded by a normal evaluation, the possibilities of neurocardiogenic syncope, carotid sinus hypersensitivity, paroxysmal bradyarrhythmia, supraventricular tachycardia, ventricular tachycardia, and many noncardiac causes still exist.
We, as future nurses should embody the knowledge, skills, and attitude in our everyday nursing practice to ensure patient’s safety and improvement of well-being.

Journal Article

Causes and Outcomes in Patients with Syncope
Syncope is a relatively common problem with a favorable prognosis in most patients. In one subgroup of patients, however, syncope denotes increased risk for serious cardiac or neurologic disease. Soteriades and coworkers used data from the Framingham Heart Study to provide some specific population-based numbers on the causes of syncope and its long-term outcomes.
The authors scanned records for 7,814 Framingham participants and found 822 subjects with reported syncope; follow-up data were available for 727 of these patients. Based on chart reviews, a physician committee excluded 120 other reported syncope cases as equivocal. To minimize recall bias, they also excluded 101 cases in which patients had not had a clinical examination in the previous four years. Other exclusions included 47 cases of syncope associated with head trauma and seven cases with incomplete records.
Four diagnostic groups were established for describing the cause of syncope: cardiac cause (e.g., ischemia, arrhythmias); neurologic cause (e.g., transient ischemic attack, stroke, seizure); unknown cause; and vasovagal or other cause (e.g., vasovagal syncope, orthostatic syncope, medication-induced syncope, syncope from cough or micturition, situational syncope).
The average age of the 822 study subjects reporting syncope was 65.8 years. The overall incidence of syncope was 6.2 cases per 1,000 person-years; the incidence increased with age and nearly doubled in the cohort of patients older than 70 years. The authors found that the most common diagnostic group was the group with vasovagal or other cause of syncope (44.9 percent), followed by the groups with unknown cause (36.6 percent), cardiac cause (9.5 percent), and neurologic cause (9.0 percent).
The average duration of follow-up available for review after a first report of syncope was 8.6 years (n = 2,181). After adjustments for age, sex, smoking, hypertension, diabetes, cardiovascular disease, use of cardiac medications, and several other relevant clinical variables, the overall risk of death from any cause was found to be 31 percent higher in the patients with syncope than in those without the diagnosis (i.e., hazard ratio of 1.31). Patients with a cardiac etiology of syncope had double the risk of death from any cause compared with patients who did not have syncope. The overall risk of death in patients with a neurologic or unknown cause of syncope was elevated to a lesser degree (hazard ratios of 1.54 and 1.32, respectively). Risk of death, myocardial infarction, or stroke was not found to be significantly elevated in the patients with vasovagal or other cause of syncope.
The authors noted that their findings supported a benign prognosis for syncope with a vasovagal cause. Their findings suggested that the small group of patients with cardiac causes of syncope should be closely monitored because of their high risk of morbidity and mortality. In addition, patients with syncope from an unknown cause may require further testing.

Soteriades ES, et al. Incidence and prognosis of syncope. N Engl J Med September 19, 2002;347:878-85, and Maisel WH, Stevenson WG. Syncope--getting to the heart of the matter [Editorial]. N Engl J Med September 19, 2002;347:931-3.

No comments: