Chapter 11 Syncope

Chart p. 389 Continued: Is it a syncopal episode? IF Yes: Loss of consciousness is transient. Patient regains consciousness spontaneously. (The syncope is self-correcting)

* Scene size-up Examine scene for safety and causes of syncope. Determine if patient was injured in fall after losing consciousness. *Initial Assessment Take spinal precautions if spinal injury is suspected. Evaluate mental status, ABCs. Administer oxygen *Focused Hist. and Phys. Exam Take SAMPLE history Interview family and bystanders. Initiate test, neurologic assessment If episode is syncopal: Continue oxygen administration, especially if signs of instability are present. Keep patient in recumbent position.

Chart p. 389 Continued: Is it a syncopal episode? IF NO: Loss of consciousness is prolonged. Patient requires resuscitation or does not regain consciousness

*Explore other (nonsyncopal) causes of loss of consciousness * Scene size-up Examine scene for safety and causes of syncope. Determine if patient was injured in fall after losing consciousness. *Initial Assessment Take spinal precautions if spinal injury is suspected. Evaluate mental status, ABCs. Administer oxygen *Focused Hist. and Phys. Exam Take SAMPLE history Interview family and bystanders. Initiate test, neurologic assessment Consider nonsyncopal causes of unconsciousness: stroke/TIA, hypoglycemia, AMI, seizure and follow treatment algorithims for these conditions.

Focused History and Physical Exam Signs and Symptoms Allergies p. 385

1. Ask to find clues: How did you feel prior to fainting? Did you have any pain or unusual sensations? Did you have any warning that you were going to faint? Did you fall or injure yourself when fainting? How do you feel now? Dizzyness is not unusual but ascertain if it is spinning or vertigo Vertigo is indicative of different pathophysiology than syncope KNOW THIS BEFORE PRECEDING. 2. Check for allergies to meds, foods, other...question if patient has been in contact with any.

Table 11-3 Conditions that mimic Syncope: Differential findings p. 388

1. Stroke: Neurologic sings and symptoms present, including slurred speech, hemiparesis, unilateral numbness, motor deficits 2. Hypoglycemia: Gradual onset, history of diabetes, unusual behavior, not transient/self correcting 3. Seizure: Patient may experience an aura prior to seizure, seizure activity observed, postical period, history of seizures, greater incidence of injury from falls than in syncope.

Orthostatic Vital Signs p. 387

3. Orthostatic Vital Signs - A 10 mmHg or greater decrease in blood pressure and a 20 bpm or greater increase in the heart rate when changing from a supine to a standing position are diagnostic of orthosatic hypotension. NOTE** Orthostatic changes after supine for 10 min. May have to wait 2 min after standing. May be significant if noted in prehospital setting. BUT its abscence does not rule out orthostasis as the cause of the syncopal episode.. Any changes of condition on standing such as the pallor, faintness, other premonitory symptoms of syncope and a positive tilt test may be considered.

Cardiocirculatory Syncope 3. Outflow Obstruction p. 382

A cardiocirculatory classification of syncope, referring to a decreased cardiac output resulting from mechanical heart valves. Underlying causes include aortic stenosis, mitral or pulmonic valve stenosis, and failure of mechanical heart valves. Circulatory obstruction may also occur as a result of pulmonary embolism, pulmonary hypertension, or pericardial tamponade. These may present with exertion syncope when there is an inability to meet the increased demand for cardiac output. Subclavian steal syndrome - may occur during arm exercises as blood flow is diverted from the cerebral circulation to the upper extremity. An unusual cause of outflow obstruction is a pedunculated atrial myxoma - a tumor attached to the atrium by a stalk-like structure whose position may intermittently cause outflow obstruction.

Cardiocirculatory Syncope 2. Orthostatic Hypotension p. 381

A form of cardiocirculatory syncope. Occurs when patient moves from a recumben or sitting position to upright Gravitational forces result in dependent venous pooling decreasing prload and cardiac output, with resultant hypotension This is not corrected by normal comensatory mechanisms. May arise from: hypovolemia, interference with compensatory reflexes, autonomic nervous system failure or a combination of these. The effect of venous pooling is exaggerated in individuals with extensive varicosities of the lower extremites.

Cardiocirculatory Syncope 1. Vasovagal and Vasodepressor Syncope explained P. 380-1

Common and tend to be familial A familiar form of vasovagal syncope occurs when a susceptible individual strains against a closed glottis, and occurs when a bowel movement or in individuals with urinary obstruction on micturition (urination) Swallowing syncope, a condition seen in patients with esophageal disease, is generally caused by vasovagal reflex mechanisms. It is believed that syncope associated with swallowing is likely related to mechanical irritation from esophageal distention or spasm. or from stimulation of associated esophageal structures such as the heart.

Cardiocirculatory Syncope continued 3. Other Cardiocirculatory Causes p. 383

Idiopathic hypertrophic subaortic stenosis (IHSS) is a chronic condition that causes progressive thickening of the left ventricle of the heart. IHSS has not been definitively linked to any specific etiology but those affected by it are believed to have a genetic predisposition. The severity of the presentation is directly related to the degree of stenosis. If there is enough stenosis, obstruction of oxygenated blood flow may be seen and the heart will be incapable of pumping enough blood to meet the body's metabolic demands. Affects ventricular septum not the free wall of the ventricle which is why the outflow obstrcution is relatively common. It is exacerbated during exertion and seen mostly in adolescents or young adults. IHSS was often called hypertrophic cardiomyopathy HCM in the past.

Cardiocirculatory Syncope continued 3. Other Cardiocirculatory Causes p. 383

In classification of cardiocirculatory syncope, both tachydysrhythmias and bradydysrhythmias can lead to decreased cardiac output and resultant synscope. Dysrhythmia-induced syncope generally occurs at heart rates less than 35 and greater than 150. These conditions are implicated: Stokes-Adams attacks, sick sinus syndrome and A-V node blocks, long Q-T syndrome, paroxysmal supraventricular tachycardia (PSVT), Wolf-Parkinson-White syndrome and ventricular tachycardia.

Cardiocirculatory Syncope continued 3. Other Cardiocirculatory Causes p. 383

In dysrhythmia-induced syncope, the dysrhythmia is paroxysma. A sustained dysrhythmia resulting in an altered mental status requires intervention to terminate the dysrhythmia. THIS IS NOT A TRUE SYNCOPE Carotid sinus hypersensitivity: A cardiocirculatory type of syncope in individuals with hypersensitive carotid sinus baroreceptive mechanism, hyperextension of the head, such as is common with shaving or tight collars. These individuals likely have a history of similar incidents.

Important note p. 383

In individuals with a hypersensitive carotid sinus, hyperextension of the head, such as with shaving or tight collars, may result in syncope

Important Note p. 384

In so called "parade square" faints, an individual standing still for a long period of time faints because of venous pooling in the lower extremities

Miscellaneous causes of Syncope p. 384

Many pharmacologic substances (See table 11-2) can result in syncope through a variety of mechanisms including cardiovascular and neurologic effects. Cough syncoope occurs due to increased intrathoracic pressure on coughing, which reduces preload and thus cardic output. Preload is also reduced by the weight of a pregnant uterus on the inferior vena cava and may occur in a recumbent or semirecumbent position. Pregnancy also results in production of hormones that lead to peripheral vasodilation which may cause syncope. Postprandial syncope , prevelent amoung elderly, occurs after meals due to gastric distension.

Mechanisms of syncope - typical findings Table 11-1 p. 380

Mechanisms: Vasovagal/Vasodepressor Causes Orthostatic Hypotension Cardiac Causes/outflow obstruction Cartoid Sinus Stimulation Metabolic Causes Neurologic Causes Miscellaneous Causes

Metabolic Syncope p. 383

Most commonly caused by hyperventilation syndrome. Noted by a period of hypoperfusion of the brain. Weight Lifter's Syncope occurs as a result of intentional preexertional hyperventilation in combination with straining against a closed glottis. Complications of diabetes mellitus may lead to syncope, either secondary to osmotic diuresis due to hyperglycemia or due to hypoglycemia. Can be cause from alcohol ingestion. (Alcohol has an inhibitory effect on the vasomotor center and inhibits antidiuretic hormone, leading to hypotension. Hypokalemia limits an increase in PVR on standing and can lead to orthostatic hypotension. (like adrenal cortical in sufficiency as in Addison's disease)

Pathophysiology of Syncope p. 379

Occurs when there is a temporaary interruption in cerebral circulation resulting in cerebral hypoperfusion. The brain, unlike some body tissues, cannot use proteins or fats for energy. There is a limited carbohydrate storage in brain Requires a constant supply of flucose for cellular metabolism Brain does not engage in anaerobic metabolism and requires an uninterrupted supply of oxygen and nutrients for energy metabolism. Brain accounts for about 20% of oxygen consumption when the body is at rest. As neuronal activity increase, so does cerebral oxyen consumption.

Initial: Focused History and Physical Exam p. 385

Physical examination and collection of the patient history in contex of knowledge of pathophysiology guides the EMS provider in differential diagnosis. It also guides prehospital management. It may not be possible to find a cause but look for significant clues. Look for findings that indicate a potentially life-threatening underlying cause such as occult bleeding or cardia dysrhythmia.

Mechanisms of syncope - typical findings Table 11-1 p. 380 Miscellaneous Causes

Possible history of coughing, pregnancy, gastric distension in the elderly, Possible use of any of a variety of pharmacologic substances (e.g., tricyclic antidepressants, quinidine, beta-blockers, diuretics, antihypertensives, neuroleptics, nitrates, ACE inhibitors, sympatholytics, phenothiazines)

Mechanisms of syncope - typical findings Table 11-1 p. 380 Neurologic Causes

Possible history of diabetic neuropathy, syphilis, alcoholic, neuropathy, other disease-related neuropathies, spinal cord lesions, surgical sympathectomy, standing still for a long period

Mechanisms of syncope - typical findings Table 11-1 p. 380 Orthostatic Hypotension

Possible history of hypotension, hypovolemia from blood loss, protracted vomiting or diarrhea, use of diuretics or inadequate fluid intake Possible use of nitrates, vasodilators, beta-blockers, calcium channel blockers, neuroleptic drugs that interfere with compensatory reflexes Possible autonomic nervous system impairment (e.g. diabetic neuropathy or age-related changes resulting in orthostatic hypotension)

Introduction to Syncope p. 378

There are many underlying pathophysiological mechanisms that may lead to the interruption of cerebral perfusion. True syncope is self-limited. Syncope resolves when the patient assumes a recumbent position, bhereby restoring cerebral circulation (see fig. 11-1 p. 378) Syncope related to paroxysmal cardiac dysrhythmia resolves on spontaneous termination of the dysrhythmia. Often preceded by prodromal symptoms, syncope is at times of such acute onset that injury is sustained from resulting fall.

Scene size-up for syncope and initial assessment Consciousness levels p. 384

These are the same for syncope You may find patient unresponsive or conscious due to the self-correcting nature of a true episode. If patient remains unresponsive for prolonged time may require resuscitation (NOT simple syncose) In this patient a more critical pathology should be considered as the cause for unresponsiveness.

Physical Exam p. 387

These may reveal important information: 1. Cardiac Monitoring - May detect borderline bradycardias or tachycardias that are still present after episode of cardiac syncope or the onset of further dysrhythmic episodes. 2. Diagnoatic quality 12-lead ECG tracings - these many indicate acute AMI or ischemia.

Medical Life Support for a patient with syncope p. 378

Three phases 1. scene size-up and initial assessment to identify and correct immediated threats to life. 2. Investigation to help determine the cause of syncope and detect injuries sustained during episode (through a focused history and physical exam) 3. Aimed at management of any treatable cause of syncope tat was discovered, including measures to prevent recurrence.

Syncope summary p. 388

Transient loss of consciousness with a loss of postural tone Self-limited because when the temporal state of cerebral hypoperfusion is corrected, consciousness returns. Most underlying causes are benign, though ominous causes and conditions may mimic syncope. A critical comparison of your findings with the pathophysiological bases of syncope will assist in establishing potential causes of syncope, tentatively ruling out other causes. Care of patient is largely supportive and aimed at preventing recurrence of the episode.

Table 11-2 Medications commonly associated with syncope p. 384

Tricyclic antidepressants Quinidine Beta-blockers Diruetics Antihypertensives Neuroleptics Nitrates ACE inhibitors Sympatholtics Phenothiazones

Mechanisms of syncope - typical findings Table 11-1 p. 380 Metabolic Causes

Typically presents with gradual onset/resolution Possible history of hyperventilation, diabetes, alcohol ingestion, hypokalemia or adrenal cortical insuffciency

Figure 11-1 p. 378

Vasovagal effects are the most common cause of syncope or fainting. The ipatient will quickly regain consciousness after assuming a recumbent position.

Prehospital management of syncope p. 387-8 Other causes of unconsciousness that mimics syncope

stroke hypoglycemia seizure these may be revealed in your assessment. See ch. 7 and 10 for more details See Table 11-3 p. 388

Interruption of cerebral perfusion is brought about by p. 379

......hypovolemia, anemia, vasodilation, mechanical obstruction of cerebral blood flow, or anything leading to reduced cardia output...including cardiac dysrhythmias, or any insufficiency, pulmonary hypertension, and decreased myocardical contractility.

Cardiocirculatory Syncope p. 380

4 Types 1. asovagal and Vasodepressor Syncope 2. Orthostatic Hypotension 3. OUtflow Obstruction 4. Other cardiocirculatory Causes

Clinical Insight p. 388

After an episode of syncope a patient will often refuse transport. Never leave such a patient alone. Always enlist someone to stay with the patient and emphasize the importance of scheduling follow-up care.

Clinical Insight p. 383

After an episode of syncope, a patient will often refuse transport. Never leave such a patient alone. Always enlist someone to stay with the patient, and emphasize the importance of scheduling follow up care.

Other Testing p. 387

Based on history and initial assessment include -neurologic assessment for signs of stroke, (such as slurred speech, unilateral weakness, facial droop. - Blood glucose testing may be useful (check history and exam to guide)

Cardiocirculatory Syncope 4. Other Cardiocirculatory Causes p. 382

Bow Hunter's stroke is a type of mechanical circulatory obstruction characterized by transitory vertebrobasilar insufficiency induced by turning the head in the presence of structural abnormalities at the craniocervical junction. Most commonly occurs in elderly as a result of cervical spondylosis, but it has been reported to have occurred due to lateral herniation of cervical intervertebral discs as well as idiopathically. Bow Hunter's Stroke may be implicated in motor vehicle crashes.

Important notes: p. 387

Cardiac monkitoring may detect borderline bradycardias or tachycardias that are still present after an episode of cardiac syncope or the onset of further dysrhythmic episodes. Keep the syncopal patient in a recumbent position and provide oxygen, especially if the patient shows persisting signs of instability.

Mechanisms of syncope - typical findings Table 11-1 p. 380 Vasovagal/ Vasodepressor Causes

Classic prodrome: dimming of vision, roaring in ears, signing or yawning, weakness, diaphoresis, pallor, nausea Possible history of stress, such as pain, bad news, sight of blood

Focused History and Physical Exam Medications Past Med. History p. 386

Current: Do you take any medications? What? Have you taken your meds today? Have you recently changed dosages of medication or started or stopped taking any? Do you take any meds. other than those prescribed by your doctor like over the counter for cold, allergy or diets? Past: Have you ever had an episode similar before? Did you seek med. attention? Have any problems as seizures, diabetes, high blood pressure, stroke or heart disease? Have been ill recently , had a fever or vomiting or diarrhea.

Cardiocirculatory Syncope Continued: 2. Orthostatic Hypotension p. 381

Diabetic neuropathy most common form of secondary autonomic failure, while age-related changes are the most common form of primary autonomic failure. Note*** In either situation, lack of autonomic regulation of vasoconstriction leads to orthostatic hypotension. ***Shy-Drager syndrome is a chronic form or orthostatic hypotension caused by autonomic failure in which plasma levels of norepinephrine do not increase on standing.

Figure 11-2 p. 381

Figure A: While the patient is lying supine, assess the heart rate and blood pressure Figure B: Place the patient in a standing or seated position and reassess the heart rate and blood pressure. An increase in the heart rate and/or a decrease in the systolic blood pressure while obtaining orthostatic vital signs may indicate volume depletion.

Syncope - a transient loss of consciousness with loss of postural tone p. 378

Greek word for fainting. A medical term for a transient loss of consciousness. It is self-correcting. Period of unresponsiveness is brief and patient will quickly regain consciousness without medical intervention. Cause of episode is usually benign and often cannot be diagnosed. EMS provider must evaluate for serious causes of syncope, such as cardiac dysrhythmias, and must be able to distinguish true syncope from other conditions that mimic syncope. If a serious causative pathology is suspected, treatment will be focused on the suspected underlying condition. If patient has apparently recovered from a sycopal episode refuses transport, it is important to ensure that the patient is not left alone and the arrangements will be made for follow up care.

Clinical Insight p. 379

If unresponsiveness is prolonged and requires resuscitative measures, the condition is, by definition, not syncope. Assessment and treatment should be focused on a more serious etiology.

Important Note p. 379

Information gathered by EMS at the scene may provide the most conclusive information ab out the cause of syncope

Mechanisms of syncope - typical findings Table 11-1 p. 380 Cardiac Causes/outflow obstruction

May occur while recumbent: may be accompanied by chest pain, palpitations Tachycardias: ventricular or PSVT (often associated with preexisting heart disease or rates >180?min) Bradycardia/tachycardia syndrome following termination of PSVT Transient episodes of reduced cardiac output (e.g., bow hunter's stroke, STokes-Adams attacks) Exertional onset associated with mechanical conditions that limit cardia output (e.g., aortic stenosis, pulmonary hypertension)

Information about syncope p. 379

Most cases are relative benign. 50% of emergency room patients who arrive for syncope do not receive a definitive diagnosis of the etiology of the episode prior to discharge. Transient in nature Difficult to diagnoses Cannot detect signs that have been resolved Require minimal intervention EMS has advantage for evaluation of the syncope Patient by arriving on the scene withing minutes of the Onset of the syncopal episode. **EMS need to make observations, obtain information and note patient assessment findings that may not be available at the emergency dept.

Neurologic Syncope p. 383

Neurologic causes of syncope include: Diabetic neurologic sequelae of syphilis, Alcoholic neuropathy Spinal cord lesions, postinfectious neuropathy of Guillain-Barre syndrome, Parkinsons's disease Riley-Day syndrome (dysautonomia, a rare hereditary disease characterized by mental retardation, incoordination and convulsions among other effect Removal of part of sympathetic nervous system ***In all of these the underlying cause of syncope is failure of vasoconsriction, resulting in perpheral venous pooling.

Cerebral understanding p. 379

No energy production in cerebral cells, they cease to carry out their functions Cerebrum is responsible for higher funtions not related to vegetative existence This results in a dysfunction of the cerebrum which disrupts consciousness. Prolonged hypoxia results in breakdown of cerebrral neuronal lysosomes These release enzymes that destroy brain cells NOTE **Any physiological derangement that leads to cerebral anoxia or prolonged hypoxia , causing prolonged unresponsiveness and requiring resuscitative measures is, by definition NOT SYNCOPE.

Important Note p. 379

Often it is the interaction of multiple factors that brings about an episode of syncope

Syncopal Eopisode Treatment pathway p. 389 (chart)

Overall Evaluation Patient loses consciousness and postural tone. Is it a syncopal episode? NO: Loss of consciousness is prolonged. Patient requires resuscitation or does not regain consciousness YES: Loss of consciousness is transient. Patient regains consciousness spontaneously. (The syncope is self-correcting)

Continued Neurologic Syncope p. 384

Parkinson's disease ruslts in a decrease of dopamine and norepinephrine, resultin in postural hypotension. Spinal cord injury, failure of th skeletal muscle pump(along with unopposed parasympathetic tone) enhances venous pooling. TIA are rarely implicated in syncope. BUT when it is it results in syncope, the mechanism by which it occurs is ischemia of the reticular activating system (RAS). Migraine headaches may be preceded by a syncopal episode especially in adolescents.

Mechanisms of syncope - typical findings Table 11-1 p. 380 Carotid Sinus Stimulation

Stimulation of oversensitive carotid sinus (e.g., by tight collar, shaving, rapid head turning) History of similar episodes

Cardiocirculatory Syncope Continued: 2. Orthostatic Hypotension p. 381

The pooling in the lower extremities triggers the compensatory mechanisms that maintain cardiac output and cerebral perfusion. Nitrates, vasodilators, beta-blockers, calcium channel blockers, and neuroleptic drugs interfere with reflex vasoconstriction and/or cardioacceleration. Autonomic nervous system impairment may be either primary or secondary.

Prehospital management of syncope p. 387-8

The question is how to treat a condition that now appears to have resolved? Keep patient in supine or semirecumbent position to prevent recurrence of the episode and potential subsequent injury (see fig. 11-5) p. 387 If a serious underlying pathology is suspected: hypovolemia or AMI, oxygen administration is indicated. intravenous fluids. venous access is also indicated if there is a potential need to administer antidysrhythmic medications, antiseizure medications r 50 % dextrose.

orthostatic hypotension p. 381

a decrease in the blood pressure or an increase in heart rate or a sensation of light headedness when a patient moves to an upright posture from a sitting or reclining positioon (or after standing still for a long time); also called postural hypotension.

Prodrome

a set of warning symptoms

carotid sinus

dilated area at the point where the common carotid artery bifurcates. It is densely supplied with sensory nerve endings that are stimulated in response to changes in pressure

vasodepressor p. 380

having the effect of depressing circulation; lowering blood pressure by dilating the blood vessels

Vasovagal p. 380

referring to action on the blood vessels caused by stimulation of the vagal nerve

Prehospital management of syncope p. 387-8 transport, refusal of care

Because of the transient nature of syncope patient may be embarrassed to accept care/transport. Explain to patient that the underlying cause of the episode needs to be investigated by a physician and underlying causes, like cardiac dysrhythmias may recur and result in death. Even with relatively benign underlying causes, another episode may recur and cause injury. If patient continues to refuse care or transport make sure someone stays with the patient and follow-up care is arranged immediately. Instruct patient in prodromal symptoms of syncope and to assume a supine or head-down position if those occur. NOTE***Documentation is critical to relieve the liability. Follow local protocols.

Scene size-up for syncope and initial assessment p. 384-5

Scene size-up Look for safety information-to see if there might be another reason for the unresponsive condition(environmental or medication) Focus on airway, breathing and circulation If potential for cervical spine injury exists or episod was unwithnessed, manually stablize cervical spin as indicated. True Syncope episode will regain consciousness <5min. May be more rapid is in recumbent position Some types of syncope are associated with gradual onset and resolution, and persistent altered mental status, it could also mean you should Steer toward a cause other than syncope. In absence of spinal injury, elevate legs to correct venous pooling and increasing level of responsiveness.

Cardiocirculatory Syncope Continued: Vasovagal and Vasodepressor Syncope explained P. 380-1

Stimulation of the vagus nerve can slow the heart rate and result in bradycardia, reducing cardia output an causing cerebral hypofusion. Vasovagal or neurocardiogenic, syncope and vasodepressor syncope, which is related to decreased PVR, typically occur in susceptible individuals in response to a stressful situation These types of syncope are accompanied by prodromal symptoms that may include a dimming or "whiting out" of the vision, a roaring noise in the ears, sighing or yawning, weakness, diaphoresis, pallor or nausea. *Can resolve without syncope in a condition called Some individuals may experience brief myoclonic activity (muscle twitching or spasm) at onset. EMS may be called for a seizure but it is not a true seizure. Brief in duration.

Cardiocirculatory Syncope continued 3. Other Cardiocirculatory Causes p. 382

Takayasu's arteritis is an inflammatory disease of the large arteries that leads to arterial stenosis and reduced blood flow through the affected arteries. Although it is rare, it is more common in adolescent and young adult females and in Asia.