Amy Gutman MD ~ EMS Medical Director www.prehospitalmd@gmail.com / www.TEAEMS.com “The only difference between syncope & sudden death is that in one you wake up”. Engel GL. Ann Intern Med 1978 “Weak & Dizzy” is a common complaint with both benign & lethal causes Etiologies of dizziness & syncope Connection of cardiovascular & neurovascular disorders Assessment & management strategies No specific “dizziness” or “syncope” protocols Protocol(s) used depends upon cause & effect(s) of symptoms A good history & physical exam provides diagnosis in most patients Not the patients to test how good you are at obtaining refusals! 82 yo WF presents with CC of “dizziness”. States intermittent, but persistent & unpredictable moments of dizziness that “made her head spin”. During the episodes, patient would nearly pass out, c/o dizziness & lightheadedness with some “blurred” vision. No CP, SOB, palpitations, seizure, loss of consciousness. No trauma, recent illness or other complaints Vitals & exam unremarkable by BLS crew. Patient initially did not want to be transported to the hospital but was convinced to get checked out. ALS crew called but unavailable What is your differential diagnosis based upon this info? History fairly unremarkable in otherwise healthy patient who recently started OTC antihistamines for sinus congestion Vitals stable but patient had at least 3 more episodes on the way to the ED in which she would lean back in stretcher & become extremely dizzy In ED, placed on a hallway bed. During her triage, while the RN had the patient on a monitor and was checking her pulse he noted the following: Syncope (Greek: sunkoptein / to cut short) Sudden & self-limiting loss of consciousness with loss of postural tone & a spontaneous recovery. A symptom, not a diagnosis Vertigo (Latin: vertere / to turn) Sensation of dizziness or abnormal motion resulting from a disorder of the sense of balance Dizzy Having a whirling sensation with tendency to fall; bewildered or confused; producing giddiness 50% with no specific causes Significant cost & time to diagnose & manage Unpredictability leads to negative impact on quality of life Management specific to the cause / suspected cause(s); varies significantly in effectiveness Syncope, dizziness & vertigo are generally symptoms rather than diseases Benign to fatal causes Cardiac causes have highest mortality rates >500,000 new patients annually 70,000 have recurrent, infrequent, unexplained syncope 3-6% ED visits annually 2-10% hospital admissions 25% Syncope Mortality 20% 15% 10% 5% 0% Overall Due to Cardiac Causes Traumatic sequellae Fever, signs of illness Focal neurological symptoms Prodromal or post-episodic Palpitations / CP SOB Seizures Nausea, Vomiting Micturition Loss of continence >2 associated with 10-20% incidence of death from neurovascular or cardiovascular causes within 1 year CAD, CHF, arrhythmia Chest pain Abnormal ECG Persistent orthostatic hypotension Age >45yrs Traumatic sequellae for any fall Cause Prevalence (Mean) % Reflex-Mediated: Vasovagal 18 Situational 5 Carotid Sinus 1 Orthostatic hypotension 8 Medications 3 Psychiatric 2 Neurological 10 Organic Heart Disease 4 Cardiac Arrhythmias 14 Unknown 34 Neurological Orthostatic 11% 24% • Vasovagal Arrhythmia • Meds • Autonomic Failure 14% • • Carotid Sinus • Peripheral vestibular dysfunction • Brainstem lesion • • Presyncope • Situational •Cough •Micturition • Non-CV 4% 12% Brady • Sick sinus • AV block • Aortic Stenosis * Tachy • VT • SVT • HOCM Long QT Unknown Cause = 34% *DG Benditt, UM Cardiac Arrhythmia Center Structural • Pulmonary HTN • Psychogenic • Metabolic • Neurological Migraine Hypoxia Hyperventilation Somatization / Psychiatric Intoxication Seizures Hypoglycemia Sleep disorders / OSA Subclavian steal syndrome Basilar artery migraine (syncope + headache) Vertebrobasilar insufficiency (syncope + vascular disease) History & Physical Exam Including ECG ENT Evaluation • Sinus CT • Otolith evaluation • Hearing exam Neurological Testing • Head CT / MRI / MRA • Carotid Doppler • EEG Metabolic • Cardiovascular • Ambulatory • Tilt Table • Echocardiogram • EPS • Angiogram • Stress Testing Psychological Evaluation Laboratory SSX: Onset & Duration Provocation or Palliation +/- & what is the reaction Medications: Allergies: Associated symptoms Sequelae Include OTCs & topicals PMH: Cardiovascular, neurovascular diseases, migraine, prior similar episodes Last Oral Intake: Events Position Medications Temperature Quality Region & Radiation Severity Loss of consciousness Time Time of day, duration of event History & physical exam leads to cause identification in nearly half of patients Sudden death Deafness Arrhythmias Congenital heart disease Heart attack or CVA at young age Seizures Metabolic disorders Serial vitals Focus on cardiac & neurologic exams Stroke scale Glucose Monitor / ECG If syncope + fall, presume a spinal injury present until proven otherwise Vasovagal Episodes after pain, fear, excitation, exertion; standing w/ locked knees “i.e. “at attention” Situational Micturition, cough, swallowing Neuralgic or Migranous Facial Pain or headache Carotid Sinus Head rotation or pressure on carotid sinus TIA / CVA Focal neurological symptoms that persist (CVA) or resolve within 172 hours (TIA); positive stroke scale Subclavian Steal Post exercise Seizure Seizure activity, LOC >5 mins with post-ictal period Murmur Presence of heart murmur on exam or echocardiogram Arrhythmia Intermittent or persistent irregularity of rhythm or regularity Psychogenic Anxiety, hyperventilating, personal gain Vertebral-Basilar Stroke Diplopia, dysarthria, dysphagia, weakness, numbness Meniere’s Aural fullness, deafness, tinnitus Brainstem evoked audiometry 95% sensitive for detecting acoustic neuromas Multiple Sclerosis Vertigo preceded by other neurologic dysfunction Psychiatric disorders Depression 25% Anxiety or panic disorder 25% Somatization Alcohol / drug abuse Personality disorder Hyperventilation Syncope & presyncope overlap CAD, CHF, PE, dysrhythmias Multisensory disorder Peripheral neuropathy Visual impairment Musculoskeletal disorder interfering with gait Vestibular disorder Cervical spondylosis Symptoms worsened with antidepressants & anticholinergics May occur while sitting, driving or position change PERIPHERAL VERTIGO CAUSES Vestibular neuronitis Labyrinthitis Meniere’s syndrome Head trauma Drug-induced CENTRAL VERTIGO CAUSES Cerebellar infarction or hemorrhage Lateral medullary infarction (Wallenberg’s syndrome) Brainstem infarction or hemorrhage Multiple sclerosis Vertebrobasilar insufficiency Aminoglycosides, phenytoin, phenobarbital, carbamazepine, salicylates, quinine Central vertigo associated with poor outcomes while peripheral vertigo is often “benign”. Can have overlap in symptoms, therefore difficult to differentiate CENTRAL ORIGIN PERIPHERAL ORIGIN Vertical, horizontal or rotary Horizontal, torsional May change direction with gaze Does not change direction with gaze change Not diminished by fixation Diminished by fixation May fatigue (if elicited by head movement) Does not significantly worsen with head movement CEREBELLAR INFARCTION Nystagmus + dizziness Horner’s Syndrome: LATERAL MEDULLARY INFARCTION: WALLENBERG SYNDROME Ptosis, Miosis, Anhidrosis Nystagmus + dizziness Nausea & vomiting Nausea & vomiting Ataxia & ipsilateral asynergia Ataxia & ipsilateral asynergia No focal weakness or motor abnormality Hoarseness Horner’s syndrome Ipsilateral facial analgesia; contralateral body analgesia No focal weakness or motor abnormality Often spontaneous Acute dizziness after neck trauma / manipulation Presents with posterior circulatory infarction symptoms MRA may reveal double-lumen, but full angiography has higher yield Neurally mediated reflex mechanism with cardioinhibitory (bradycardia) & vasodepressor (hypotension) components Vasovagal syncope (VVS) Carotid sinus syndrome (CSS) Situational syncope Loss of the normal balance between sympathetic & parasympathetic nervous system Triggered by stretch & mechanoreceptors (carotid sinus, bladder, esophagus, respiratory tract) Peripheral venous pooling causes sudden decreased venous return Pallor, nausea, sweating, palpitations common Rare except in elderly “Falls after losing balance” Sensory nerves in carotid sinus walls respond to stimulation increasing afferent signals to brain stem Reflexive increase in efferent vagal activity & decreased sympathetic tone results in bradycardia & vasodilation Different syndrome than carotid sinus hypersensitivity, similar management Drug-induced Primary autonomic failure Deconditioning, parkinsonism Secondary autonomic failure Often from diuretics, vasodilators Diabetes +/- neuropathy, amyloidoisis Alcohol Orthostatic intolerance +/neuropathy Decline of >20mmHg SBP or 10mmHg DBP from supine to standing Elderly vulnerable due to decreased baroreceptor sensitivity, decreased cerebral blood flow, increased renal sodium wasting, decreased thirst response with aging Peripheral sympathetic tone impairment due to diabetic neuropathy, anti-HTN medication Non-contrast CT helps r/o acute hemorrhage (but not 100% accurate) MRI more sensitive than CT for hypoxic injury or cerebellar & brain-stem infarctions PET scan may improve diagnostic accuracy CT angiography or MRA useful within 24 hours Carotids often included in evaluation Not 1st line testing Differentiates syncope from seizures Evaluates NMS predisposition Specificity of negative test 90% Nystagmus & vertigo with peripheral lesions when diseased side turned downward Peripheral nystagmus may fatigue with repeated maneuvers Central lesions not significantly changed with position change Symptoms of peripheral nystagmus dramatically worsened with head movement & tends to fatigue with repeated maneuvers PERIPHERAL VERTIGO CENTRAL VERTIGO Time before onset of nystagmus 2-20 secs 0 secs Duration of nystagmus <1 min >1 min Fatiguability Yes with repetitiion Non-fatiguiing Direction of nystagmus Upbeat & torsional May change direction Intensity of vertigo severe Minimal to moderate • Potential consequence is carotid occlusion / clot resulting in stroke LOC often w/o prodrome Significant injury risk Structural heart disease is most important risk factor for predicting risk of death from syncope or dizziness Acute MI / Ischemia Hypertrophic cardiomyopathy Aortic dissection Pericarditis Pericardial tamponade Pulmonary embolus Pulmonary HTN Aortic stenosis Atrial myxoma Bradyarrhythmias Tachyarrhythmias Normal or abnormal? Normal “now” does not equal normal “always” Fast or slow? Pauses? Pacemaker? Holter 24-48 hours symptoms w/ arrhythmia (5%) v. symptoms without arrhythmia (17%) External Loop Event Recorder Weeks to months Limited value in sudden LOC Loop Recorder Months Implantable type more convenient Provided diagnosis in 55% of pts with unexplained syncope compared to conventional methods From the files of DG Benditt, UM Cardiac Arrhythmia Center Wide, weird & slow Sinus brady Symptomatic 1st degree HB 3rd degree HB Cause often correctible with medication adjustment Indication for atrial pacemaker implantation Ventricular pacing indicated in atrial fibrillation with slow ventricular response Bradycardia 36% NSR 58% Tachycardia 6% Ventricles depolarizing on their own because of no atrial conduction Rate between 20-40 Rate of 60-120 (all PVCs) often called “Slow VT” Diagnostic clue: no p waves or flipped p waves in all leads Wide, weird & fast or narrow & regular Regular or irregular, intermittent or persistent Cause often structural, ischemic & pathologic – not easily corrected with a simple medication change Surgery (if related to stenosis or CAD) +/- ventricular pacing often indicated Risk of sudden cardiac death AKA: Ventricular extrasystole, premature beat, ectopic beat, premature depolarization Occasional monomorphic PVCs common in normal hearts but also seen in the setting of heart disease Polymorphic VT never normal Ischemia, metabolic or structural disorders QT widens to point when a PVC occurs early in the cardiac cycle falling on the apex of preceding T wave leading to VT or torsades Antiarrhythmics Psychoactive Agents Erythromycin, Pentamidine, Fluconazole Antihistamines Phenothiazines, Amitriptyline, Imipramine, Ziprasidone Antibiotics Class IA & III: Quinidine, Procainamide, Sotalol, Amiodarone Terfenadine, Astemizole Others Cisapride, Droperidol VENTRICULAR TACHYCARDIA Abnormal tissues in ventricles generating rapid & irregular rhythm >3 PVCs in a row; can be sustained or unsustained Rhythm: Regular Rate: 150-250bpm QRS Duration: Prolonged >120ms P Wave: Not seen, often dissociated VENTRICULAR FIBRILLATION Disorganized electrical signals cause ventricles to quiver ineffectively Rhythm: Irregular Rate: >250, disorganized QRS Duration: Unrecognizable P Wave: Not seen Patient emergently trans-thoracially paced in ED while receiving fluid boluses & amiodarone Went to OR for permanent dual-chamber (atrial & ventricular) pacemaker Patient’s antihistamines discontinued (unclear if contributed to symptoms) Discharged home a few days later with no permanent sequellae Ventricular > atrial > dual chamber Most pacemakers are “demand” type EKG shows a “spike” when pacer fires Beware the patient with a pacemaker, syncope / dizziness with no pacer spikes on EKG! Recognize symptoms & avoid provocation Avoid alcohol, lack of sleep, environmental stressors Adequate hydration & food intake Avoid drugs that lead to hypotension Avoid activities that precipitate syncope Preventing LOC or Injury Supine position upon onset of prodrome Avoid driving or other activities that could lead to injury Cardiovascular / neurovascular interventions Routine follow-up Take prescribed medications as prescribed! Dubin’s Guide to EKGs. Images: Wikipedia, Google, Bing searches. www.UpToDate.com. “Dizziness”, “Syncope”, “Ventricular Tachyarrythmias”. 2013. D. Okorn MD. “Approach to Dizziness”. Swedish Family Medicine. Dec 2009 G. Bergey MD. “Acute Dizziness & Vertigo: Diagnosis, Assessment and Management”. 2001 M. Lehmann MD. “Tacchyarrythmias”. 2010 E. Veiga, M.D, 2008 WN Kapoor. Syncope. NEJM 2000; 343: 1856-62 Freeman, R. “Neurogenic Orthostatic Hypotension” NEJM 2008; 358: 615-624 Soteriades, et al. Incidence and Diagnosis of Syncope. NEJM 2002; 347:878-885 Grubb, B. Neurocardiogenic Syncope. NEJM 2005; 1004-1010 DG Benditt. “Syncope - A Diagnostic & Treatment Strategy”. Royal Brompton Hospital, London, UK Kapoor W, Med. 1990;69:160-175 JJ Blanc, et al. Eur Heart J, 2002; 23: 815-820 WN Kapoor. “Evaluation and outcome of patients with syncope”. Medicine 1990;69:160-175 History & exam important in providing or eliminating a diagnosis Most causes benign & self-limited but almost impossible to make a prehospital diagnosis Serious causes suspected by abnormal CV or neuro exam Recognize stroke syndromes that may present with dizziness as a prominent feature