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Syncope in elderly

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  1. 1. 1 SYNCOPE • Syncope is a sudden loss of consciousness and postural tone resulting from a decrease in cerebral blood flow. The loss of consciousness is brief, and recovery is rapid and spontaneous. • Syncope itself is not a diagnosis but rather a symptom of an underlying disorder. EPIDEMIOLOGY: • The incidence of syncope increases dramatically with advancing age. • The incidence of syncope per 1000 person-years increases from 6 in the sixth decade of life to 11 in the seventh decade. The incidence is 17 and 20 for men and women, respectively, in the eighth decade. • Almost 50% of emergency room visits for syncope are made by persons 65 years of age or older. • Subjects with cardiac, neurologic, or unknown causes of syncope have a worse prognosis than subjects without syncope. Interestingly, subjects with vasovagal, orthostatic, or medications as a cause of their syncope did not have a decreased survival compared with subjects without syncope. PATHOPHYSIOLOGY: • The underlying pathophysiology leading to syncope is inadequate oxygenation of the cerebral cortex and reticular activating system, resulting in loss of consciousness. Risk factors for increased syncope in elderly: • Having more underlying chronic conditions and being on more medications than younger adults. • age-related physiological changes that increase their syncope risk: 1. Atherosclerosis (impairing dilation of cerebral blood vessels in the face of reduced blood flow) 2. Increased endothelin production (increasing vasoconstriction of cerebral arterioles) 3. Left ventricular dysfunction, due to long standing hypertension and/or heart disease (causing decreased cardiac output) 4. Cardiac valvular disease (increasing the likelihood of arrhythmias and heart block)
  2. 2. 2 5. Blunting of autonomic responses, baroreceptor reflex (predisposing the person to orthostatic hypotension) CAUSES: • They fall into these general categories: neurally mediated (reflex) causes, orthostatic hypotension, cardiac causes, central nervous system diseases, and psychiatric disorders. EVALUATION: A) HISTORY:
  3. 3. 3 • History from the patient and an eyewitness, if present, is needed to distinguish syncope from other entities such as dizziness, vertigo, drop attacks, coma, and seizure. • Historical features are often sufficient to distinguish syncope from seizures. Seizures are associated with blue face (or not pale), frothing at the mouth, tongue biting, disorientation, aching muscles, sleepiness after the event, and duration of unconsciousness of more than 5 minutes. On the other hand, symptoms associated with syncope are sweating or nausea before the event and being oriented after the event. The best discriminatory symptom is disorientation after the episode, which often signifies a seizure.
  4. 4. 4 • Vasovagal or neurocardiogenic syncope is the most common type of neurally mediated syncope; it includes the common faint. Typically, a situation involving prolonged standing, emotional distress, or exertion in a warm environment causes peripheral venous pooling and a drop in blood return to the heart. As the heart recognizes a sudden decrease in preload, it tries to compensate by contracting harder. The quick increase in contraction activates mechanoreceptors in the ventricles that start a reflex mechanism causing the central nervous system to stimulate vasodilation and bradycardia. As the drop in cardiac output becomes more profound, syncope may occur.When suspecting a neurally mediated syncope, look for associated symptoms of nausea and/or vomiting, prolonged standing, hot environments, and unpleasant situations. You should be cautious to not assume this diagnosis in patients with known heart disease or repetitive episodes of syncope. • Carotid sinus syndrome: when manual stimulation of the carotid sinus can, in susceptible individuals, stimulate neurally mediated syncope. • Orthostatic hypotension: is a drop in arterial pressure that occurs when an individual moves to an upright position. Typically, the autonomic nervous system rapidly compensates for this by increasing the venous tone in the legs; when this system fails, syncope may occur. When the circulating blood volume is depleted, as in dehydration, orthostatic hypotension, and syncope may occur even with appropriate autonomic compensation. This diagnosis should be considered in individuals who are on medications that can predispose to hypotension, who have reason due to illness or blood loss to be dehydrated, or have autonomic insufficiency from a neurological disorder such as Parkinsonism. A typical case occurs soon after standing up • Cardiac syncope occurs when reduction in cardiac functioning by arrhythmia, death of myocardium, or outflow obstruction leads to decreased blood flow to the brain. Several studies have shown an increase in overall mortality and sudden death among patients with cardiac syncope compared to patients with syncope from other causes. A cardiac cause should be considered when syncope is preceded by palpitations or chest pain, or when it occurs during exertion. Patients with known severe structural heart disease should be considered to have cardiac syncope until proven otherwise.
  5. 5. 5 • Cerebrovascular disease is a rare but plausible cause of syncope. Most transient ischemic attacks or strokes do not cause loss of consciousness, but occasionally this can occur. There is a low yield to use of neurological testing in the evaluation of individuals with syncope unless it is directed at those with neurological findings on initial evaluation. • Psychiatric causes should be considered in patients with repetitive syncope of unknown origin after cardiac causes have been effectively ruled out. They are more common in younger patients. Prodromal symptoms, such as dizziness, are common. Several hypotheses exist regarding the connection between psychiatric disorders and syncope. Hyperventilation can increase susceptibility to neurally mediated syncope. There is also a term called pseudo- syncope, which has been used to describe patients with syncope of unknown but presumed psychiatric origin, who have no pathological findings on exam and documented syncope without any change in blood pressure or pulse. The history can identify symptoms and situations surrounding syncope that can help diagnose three common etiologies, neurally mediated (vasovagal), orthostasis, and drug related syncope. B) PHYSICAL EXAMINATION: • .In detection of orthostatic hypotension, supine blood pressure and heart rate should be measured after the patient has been lying down for at least 5 minutes. Standing measurements should be obtained immediately and for at least 3 minutes. Sitting blood pressures are not reliable for detection of orthostatic hypotension. • Several cardiovascular findings are crucial diagnostically. Differences in the pulse intensity and blood pressure (generally >20 mmHg) in the two arms are suggestive of aortic dissection or subclavian steal syndrome. • Special focus on cardiovascular examination for aortic stenosis, • Carotid Bruits, carotid massage. • Neurological examination. The evaluation of the patient with syncope involves the parallel process of seeking a specific diagnosis and ruling out cardiac causes. The initial history,
  6. 6. 6 examination, and electrocardiogram are sufficient in most cases to rule in or out cardiac disease C) Further evaluation: Should focus on the following issues: (1) arrhythmia detection, (2) tilt testing, and (3) multiple abnormalities causing symptoms.  Arrhythmia Detection  Electrocardiogram or a rhythm strip  Ambulatory holter monitoring  Electrophysiologic studies  External loop recorders  Implantable loop recorders. Cardiac stress testing is rarely diagnostic in the evaluation of syncope. It should be considered in patients who have syncope during exertion or experience chest pain associated with syncope.  Tilt table testing:  Can be useful as confirmatory tests for neurally mediated syncope.  The procedure involves baseline measurement of blood pressure and heart rate while supine, then quickly bringing the patient to an upright position by tilting to approximately 60 degrees. A foot board is in place for support. The patient is then kept in the tilted position for 45 minutes to observe for syncope or presyncopal symptoms while continuing to monitor heart rate and blood pressure. Some protocols include giving isoproterenol or nitroglycerin after the patient has been asymptomatic in the tilted position for 10 to 15 minutes followed by further monitoring. If syncope symptoms occur during testing and correlate with a quick drop in blood pressure or pulse rate, it is considered a positive test. Likewise, if syncope occurs without a change in vital signs, a neurally mediated syncope is less likely and other etiologies should be reconsidered  Carotid massage: CSM is performed as follows: 1. Confirm that no carotid bruits are present and that there is no known significant cerebral vascular disease. If bruits are present, or the patient is at high risk for atherosclerotic disease, consider carotid Doppler ultrasound to evaluate for significant plaque. 2. Have the patient supine, on continuous ECG monitoring and beat-to-beat blood pressure monitoring. An IV line should be in place, and atropine and transcutaneous pacing available. 3. Turn the patient’s head to the left in the supine position and find the maximum impulse in the right carotid artery at the level of the thyroid cartilage. Use two fingers, firmly press down,and massage longitudinally for 5 to 10 seconds. Wait a few minutes and repeat on the left carotid sinus. Repeat in the head-up tilt position if symptoms do not occur in the supine position.
  7. 7. 7 A positive cardioinhibitory result is present if a cardiac pause (asystole) of 3 seconds or longer occurs during or immediately after CSM; a positive vasopressor result is present if the systolic blood pressure drops 50 mmHg or more, and is accompanied by symptoms.  Multiple abnormalities causing symptoms:  According to the published recommendations for syncope evaluation, neuroimaging and EEG can be limited to patients with symptoms or signs of acute stroke or seizure.  Initial laboratory blood tests rarely yield diagnostically helpful information. Hypoglycemia, hyponatremia, hypocalcemia, or renal failure is found in 2% to 3% of patients, but in most cases appears to result in seizures rather than syncope .
  8. 8. 8 MANAGEMENT:  Management Considerations o Management issues include hospitalization decision, treatment selection, and patient instructions and education. o the treatment largely depends on the cause of syncope. o First-time syncope in patients without known or suspected heart disease usually warrants the reduction of risk factors for further syncope. This includes reducing polypharmacy and medication misuse, treating underlying illness, and education regarding avoidance of triggers. o Individuals with cardiac disease deserve a more aggressive effort in establishing an etiology of syncope and treatment of cardiac causes. Identifying and treating structural heart disease will help reduce the risk of recurrent syncope. When to Hospitalize o Consider hospitalization of older patients with multiple comorbidities when the etiology seems multifactorial and a monitored environment is needed to sort it out. o Hospitalize patients with known or suspected potentially fatal arrhythmias. o Hospitalize patients with unknown etiology of syncope when cardiac disease is known or suspected by initial evaluation.
  9. 9. 9 o Hospitalize when the cause is identified and requires admission (e.g., myocardial infarction or pulmonary embolism the treatment according to the cause of syncope Neurally Mediated Syncope o Because of potential side effects, treatment should be reserved for elderly patients with frequent or disabling symptoms. Because psychiatric illnesses (especially depression and anxiety) probably lead to vasovagal reactions, screening for the psychiatric illnesses noted above should be performed. Treatment of the psychiatric illness often results in resolution of recurrent syncope. o The most commonly used drugs are beta-blockers (e.g., metoprolol 50–200 mg/day, atenolol 25–200 mg/day, and propranolol 40–160 mg/day), which may inhibit the activation of cardiac mechanoreceptors by decreasing cardiac contractility. Other drugs include anticholinergic drugs, such as transdermal scopolamine one patch every 2 to 3 days, disopyramide (200 –600 mg/day), paroxetine (20–40 mg/day) theophylline (6–12 mg/ kg/day), and measures to expand volume (increased salt intake, custom fitted counter pressure support garments from ankle to waist, and fludrocortisone acetate at 0.1–1 mg per day). Orthostatic Hypotension o The initial approach to treatment of orthostatic hypotension is to ensure adequate salt and volume intake and to discontinue drugs that cause orthostatic hypotension. Patients with orthostatic hypotension should be advised to raise the head of the bed at night, to rise from bed or chair slowly, and avoid prolonged standing. Compressive stockings applied up to thigh level may help decrease venous pooling. Frequent small feedings may be helpful for patients with marked postprandial hypotension. o Pharmacologic agents of potential benefit include fludrocortisone (0.1–1 mg/day), in conjunction with increased salt intake. Various agents have been used including midodrine, ephedrine, phenylephrine, and others. Patient Instructions and Education o Issues in patient education include instructions in prevention of syncope, nonpharmacologic treatment, and restriction of activities. Many patients with vasovagal syncope have precipitating factors or situations that should be identified, and the patient instructed to avoid these situations. Common triggers include prolonged standing, venipuncture, large meals, and heat (such as hot baths or sunbathing). Additionally, fasting, lack of sleep, and alcohol intake may predispose to vasovagal syncope and should be avoided. o Post exercise vasovagal syncope may occasionally be related to chronic inadequate salt and fluid replacement. Syncope may be prevented with the use of electrolyte containing solutions and water in such instances. In other patients exercise may have to be curtailed. Finally, do not forget to think of safety issues such as driving, flying, operating heavy machinery, and risk of injury from falls.
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