DOCSLIB.ORG

Neurally Mediated Syncope

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Neurally Mediated Syncope Neurol. Croat. Vol. 62, 1-2, 2013 Neurally mediated syncope A. Ljilja1, A. Mišmaš2, I. Adamec2, M. Habek1,3 ABSTRACT - Neurally mediated or vasovagal syncope is the most common cause of transient loss of con- sciousness. Too excessive response to diff erent triggers (emotional stress, scenes of blood, prolonged stand- ing, etc.) results in brief and self-limiting loss of consciousness caused by a sudden drop in blood pressure with or without heart rate drop, which leads to transient brain hypoxia. Prior to the episode of syncope, the patient can have a sensation of nausea, sweating, pallor, and visual fi eld narrowing. Although it is known that in the syncope background there is dysregulation of blood pressure control, the pathophysiology is still un- clear. Blood pressure regulation involves complex aff erent signals from the aortic arch processed by the cen- 3 tral nervous system and eff erent modulation of the heart and vascular system. Vasovagal syncope usually 1-2, 2013 Number does not require treatment. However, in some cases to rule out other causes of fainting, such as arrhythmias, a broad diagnostic work-up is required, for which head-up tilt table test is most commonly used. Frequent vasovagal syncope adversely aff ects patient’s quality of life and pharmacological treatment with β-blockers, such as metoprolol, selective serotonin reuptake inhibitors and vascular constrictors like α-agonists can be administered. Other techniques to reduce hypotension are foot exercise, compressive stockings, increased fl uid and salt intake. In more serious cases of vasovagal syncope with bradycardia or asystole, insertion of the electric pacemaker is an option. Key words: bradycardia, head-up tilt table test, hypotension, neurally mediated syncope INTRODUCTION 1School of Medicine, University of Zagreb, Zagreb, Syncope is a transient loss of consciousness with Croatia complete and fast recovery of consciousness and 2Zagreb University Hospital Center, Clinical Depart- previous neurological functions. In general, it can ment of Neurology, Referral Center for Intensive Neu- rology of the Croatian Ministry of Health, Zagreb, be classifi ed as vasovagal (situational, neurally me- Croatia diated), cardiac or orthostatic syncope. Older pa- 3Zagreb University Hospital Center, Clinical Depart- tients are more prone to orthostatic syncope, ca- ment of Neurology, Referral Center for Demyelinating rotid sinus hypersensitivity and cardiac syncope, Diseases of the Central Nervous System of the Croatian while younger patients are more prone to vasova- Ministry of Health, Zagreb, Croatia A. Ljilja, A. Mišmaš, I. Adamec, M. Habek. Neurally mediated syncope Neurol. Croat. Vol. 62, 1-2, 2013 gal syncope (VVS). Other syndromes with similar Aff erent signals are transmitted from the aortic presentations are seizures, metabolic and psycho- arch via vagal nerve and from the carotid sinus via genic disorders, and acute intoxication. glossopharyngeal nerve to the central nervous sys- tem. Distension of the vascular structures aft er car- Patients with frequent episodes have greater pos- diac systole results in discharge of aff erent nerves sibility of severe clinical disorders compared to pa- that converge from the nucleus tractus solitarius to tients with isolated syncope (1). VVS is a common the brainstem. At this point, eff erent sympathetic problem in the population. About 3.5% of people fl ow is inhibited and eff erent vasovagal fl ow is in- experience one or more episodes of VVS in life- creased (10). time (2). Approximately 40% of cases remain undi- agnosed, while 30% of patients experience recur- Th e most commonly used model for the neurally rent episodes (3). Th e pathophysiology of syncope mediated syncope is the Bezold-Jarisch refl ex in is a complex hemodynamic response with marked which excessive venous load begins a chain of hypotension, bradycardia and loss of conscious- events that culminate in vasodilatation and brady- ness. Syncope is caused by barorefl ex dysfunction, cardia, which consequently leads to hypotension neuroendocrine response, and inadequate respon- and loss of consciousness (11). se of the central nervous system to stressor. Epi- Excessive venous load of the lower extremities re- sodes of syncope in today’s lifestyle can cause dis- sults in decreased ventricular volume, which acti- comfort and inconvenience for the patient. In most vates sensory receptors in the inferoposterior wall cases, medical history, physical examination and of the left ventricle, which responds to pressure standard electrocardiogram (ECG) are suffi cient changes by increasing nerve outfl ow to the central for diagnosis (3). Although there are many diff er- nervous system via vagal nerve. Parasympathetic ent therapeutic measures to prevent syncope, its activity accompanied by vasodilatation and brady- treatment is largely empirical and suboptimal, cardia increases (12). It is believed that diff erent which is a result of heterogeneous patient popula- modulators of the central nervous system activity tion and the lack of controlled randomized trials can cause vasovagal syncope. Th e potential media- (4). In most cases, detailed medical history is tors in the development of vasovagal syncope are enough to determine the causes of fainting. Th e serotonin, adenosine and opioids. Th e β endorphin term ‘pre-syncope’ is used to describe a situation level is increased in patients during syncope. Dif- that resembles the prodromes of syncope, but is ferent clinical presentations of vasovagal syncope, 4 not followed by loss of consciousness. It is believed variable outcome and syncope induced by the tilt- that the pathophysiological mechanisms of pre- up test with drugs, such as isoproterenol, nitro- syncope are the same as in syncope (5). glycerin and clomipramine indicate that complex pathophysiological mechanisms cause vasovagal Epidemiology reaction. Syncope is a common clinical disorder with the Number 1-2, 2013 Number Neurohumoral theory annual incidence of 1.3 to 2.7 per 1,000 inhabitants (2). Epidemiological studies indicate that approxi- Experimental models have shown that the injec- mately 40% of people in the general population tion of serotonin into cerebral ventricular areas have experienced at least one episode of syncope can cause similar sympathetic withdrawal response (6). Clinical studies show that the peak incidence as in vasovagal syncope (13,14). Selective serotonin of syncope is between 10 and 30 years of age (7). In reuptake inhibitors (SSRI) can be successful in the younger patients, neurally mediated syncope is the treatment of vasovagal syncope (15). Some authors most common cause, whereas in older patients suggest that because the SSRI facilitate nerve trans- cardiovascular causes are more frequent (8). mission, they cause SSRI receptor down-regulation in the brainstem, which results in a blunted re- sponse to rapid shift s in the central serotonin levels Etiology and pathophysiology (15-18). Physiological regulation of blood pressure consists of the aff erent signals processed by the central Dysregulation of cerebral fl ow nervous system, and the eff erent modulation of the cardiovascular system (9). Normal regulation of More than 35 years ago, some authors suggested arterial blood pressure is controlled by barorecep- the patients with VVS to have abnormal cerebral tors located in the aortic arch and carotid sinus. vascular response to orthostatic stress, which may Neurol. Croat. Vol. 62, 1-2, 2013 A. Ljilja, A. Mišmaš, I. Adamec, M. Habek. Neurally mediated syncope be associated with the pathophysiology of this syn- than half (56%) had a history of mood disorder drome (19). Th is concept is supported by fi ndings and 21% were taking psychotropic medications. on cerebral vasoconstriction and reduced cerebral Psychological problems include suicidal thoughts, blood fl ow in patients with VVS. depression, panic attacks and chronic anxiety, which is similar to the level of emotional symptoms in chronic patients. CLINICAL PRESENTATION History data on environmental factors are impor- DIAGNOSTIC EVALUATION tant for the diagnosis, since syncope is oft en caused by the sight or loss of blood, sudden stressful or Th erapeutic and diagnostic guidelines of the Euro- painful experience, surgical manipulation or trau- pean Society of Cardiology defi ne standards for ma. Precipitating symptoms and signs are pallor, the management of syncope and propose a model weakness, yawning, nausea, hyperventilation, blur- of organization for patient evaluation (23). Blood red vision and impaired hearing immediately be- tests, cardiac workup (ECG, echocardiography, fore syncope. Th e patient falls in horizontal posi- holter ECG), head-up tilt table test (HUTT), elec- tion and aft er a few seconds or minutes returns to troencephalography (EEG), transcranial vessel ul- consciousness. While regaining consciousness, the trasound and neuroimaging are diagnostic proce- patient may experience a feeling of weakness, but dures for syncope. Despite all clinical tests, the usually does not show signs of confusion. VVS is cause of syncope remains undetermined in 30% of mostly associated with benign prognosis. A small patients. proportion of patients have recurrent attacks of syncope, which can aff ect their quality of life, HUTT allows for reproduction of syncope and mainly due to frequent falls and injuries (20). monitoring the patient’s physiological responses during syncope. Direct observation and documen- Although most patients shows typical signs of VVS tation
Load more

Recommended publications
  • Clinical Presentation of Orthostatic Hypotension in the Elderly
    Postgrad Med J: first published as 10.1136/pgmj.70.827.638 on 1 September 1994. Downloaded from Postgrad Med J (1994) 70, 638 - 642 © The Fellowship of Postgraduate Medicine, 1994 Medicine in the Elderly Clinical presentation oforthostatic hypotension in the elderly G.M. Craig Formerly Consultant Geriatrician, Northampton Health Authority, Northampton, UK Summary: Fifty cases of orthostatic hypotension in the elderly are analysed. Three main modes of presentation were identified: (1) falls or mobility problems; (2) mental confusion or dementia; or (3) predominantly cardiac symptoms. Selected case histories are given to illustrate diagnostic difficulties. Medication was responsible for orthostatic hypotension in 66% of patients and striking examples of polypharmacy were encountered. However, 34% of cases were not iatrogenic. Only 14% of patients had overtly postural symptoms. A high index ofsuspicion is needed to diagnose orthostatic hypotension in the elderly and the condition is often overlooked. The paper provides useful diagnostic clues for clinicians. Introduction Orthostatic hypotension is common in hospital reason the patients' age is not on record in ten The condition in cases. With this proviso the mean age was 80 years geriatric practice. may present by copyright. unusual ways in the elderly and can easily be (n = 40, range 63-97 years). There were 24 men overlooked. Some cases are a consequence of and 26 women in the series. autonomic failure. Physiological and pathology aspects, and treatment of autonomic failure are quite well covered in the literature.'I Detailed tests Clinical presentation have been devised to locate the precise level of neuronal dysfunction once the diagnosis has been The presenting features in order of frequency are established6 and the clinical features have been well shown in Table I.
    [Show full text]
  • Evaluation and Management in an Urgent Care Setting
    Syncope Evaluation and Management in an Urgent Care Setting Urgent message: When a patient presents to urgent care after a syncopal event, the clinician’s charge is to determine whether the episode was of benign or potentially life-threatening etiology and whether the patient should be transferred for further evaluation. Kenneth V. Iserson, MD, MBA, FACEP, FAAEM, Professor of Emergency Medicine, The University of Arizona, Tucson, AZ Introduction yncope is a sudden, transient loss of consciousness with a loss of postural tone (typically, falling). It results from an abrupt, transient, and diffuse cerebral Smalfunction and is quickly followed by sponta- neous recovery. The term syncope excludes seizures, coma, shock, or other states of altered consciousness. Many patients will ascribe their syncopal episode to a sit- uationally mediated vasovagal episode. Despite this, the goals in the urgent care setting include the following: Ⅲ Determining whether the patient’s episode was actually a syncopal or presyncopal event, and if it could have a life-threatening etiology Ⅲ Stabilizing the patient Ⅲ Transferring those patients who need further diag- nostic studies or therapeutic interventions © John Bolesky, Artville © John Bolesky, Epidemiology Syncope accounts for up to 3% of emergency depart- common in young adults, while cardiac syncope ment (ED) visits and up to 6% of hospital admissions becomes increasingly more frequent with advancing each year in the United States.1,2 At some time in their age.4 The chance of having at least one syncopal episode lives, up to about half the population (12% to 48%) of in childhood is between 15% and 50%.5 Though a people may experience syncope.3 benign cause is usually found, syncope in children war- Syncope occurs in all age groups, but it is most com- rants prompt detailed evaluation.6 mon in adults.
    [Show full text]
  • Syncope in Adults: Systematic Review and Proposal of a Diagnostic and Therapeutic Algorithm
    International Journal of Cardiology 162 (2013) 149–157 Contents lists available at SciVerse ScienceDirect International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard Review Syncope in adults: Systematic review and proposal of a diagnostic and therapeutic algorithm Salvatore Rosanio a,⁎, Ernst R. Schwarz b, David L. Ware c, Antonio Vitarelli d a University of North Texas Health Science Center (UNTHSC) Department of Internal Medicine, Division of Cardiology 855 Montgomery Street 76107 Fort Worth, TX, United States b Cardiology Division, Cedars Sinai Medical Center, Los Angeles, CA, United States c Cardiology Division, University of Texas Medical Branch, Galveston, TX, United States d Cardio-Respiratory Department, La Sapienza University, Rome, Italy article info abstract Article history: This review aims to provide a practical and up-to-date description on the relevance and classification of syncope Received 19 June 2011 in adults as well as a guidance on the optimal evaluation, management and treatment of this very common clin- Received in revised form 28 October 2011 ical and socioeconomic medical problem. We have summarized recent active research and emphasized the value Accepted 24 November 2011 for physicians to adhere current guidelines. A modern management of syncope should take into account 1) use of Available online 20 December 2011 risk stratification algorithms and implementation of syncope management units to increase the diagnostic yield and reduce costs; 2) early implantable loop recorders rather than late in the evaluation of unexplained syncope; Keywords: fi Syncope and 3) isometric physical counter-pressure maneuvers as rst-line treatment for patients with neurally- Pacing mediated reflex syncope and prodromal symptoms.
    [Show full text]
  • Dizziness: If Not Vertigo Could It Be Cardiac Disease?
    Cardiology Dizziness: if not Maja Susanto vertigo could it be cardiac disease? Background Case study Dizziness is a common presentation in general practice. A woman aged 75 years presented to the emergency However, the symptom of dizziness represents a spectrum of department with recurrent dizziness and fainting pathology from benign to serious. episodes. Objective Dizziness is a common presentation that accounts for about 5% This review provides an evaluation of a patient presenting of primary care visits.1 When a patient describes dizziness, it can with presyncope/syncope. reflect one of four conditions (Table 1).1,2 Unfortunately, patients Discussion tend to use the term dizziness loosely. In the case study described in Dizziness can be a symptom of one of four conditions: vertigo, this article, the patient presented with dizziness followed by fainting presyncope, disequilibrium or light-headedness. It is often episodes, indicating presyncope rather than vertigo. unclear what patients mean by dizziness as they use this term loosely. Hence, clinicians must be vigilant in evaluating She had a history of hypertension, stable familial patients presenting with dizziness and be mindful of red flags haemochromatosis, gastroesophageal reflux disease and that may indicate serious pathology. This review begins with hypothyroidism, which was treated with thyroxine but a case study describing the wide range of causes of dizziness. treatment was ceased due to euthyroid status. She is a Careful history taking and physical examination are pivotal in lifelong non-smoker and drinks three glasses of wine each evaluating patients presenting with dizziness. day with dinner. Her medications include lercanidipine Keywords 20 mg daily, irbesartan 150 mg daily and omeprazole 20 dizziness; diagnosis, differential; heart diseases mg daily.
    [Show full text]
  • If It's Not Epilepsy
    J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.70.suppl_2.ii9 on 1 June 2001. Downloaded from J Neurol Neurosurg Psychiatry 2001;70(suppl II):ii9–ii14 IF IT’S NOT EPILEPSY . .Banner Philip E M Smith *ii9 he most important diagnostic problem in epileptology is to distinguish epileptic seizures from syncope and from psychogenic attacks. A less common problem is the need to distin- guish epilepsy from other paroxysmal disorders with which it may overlap. Improved T 1 understanding of ion channel disorders has blurred the definition of epilepsy. The diagnosis of episodic altered consciousness rests largely with the clinical history, notwithstanding the remarkable advances in the technology of imaging and neurophysiology. Common reasons for misdiagnosis are: c inadequate or missing history—for example, no witness c clonic movements or incontinence accompanying syncope or psychogenic attacks c undeserved emphasis on a family history of epilepsy or a history of febrile convulsions c overinterpretation of minor electroencephalography (EEG) abnormalities or normal age specific variants. c SYNCOPE Syncope is the most common “non-epileptic” cause of altered consciousness. The two main types are reflex (vasovagal) and orthostatic syncope. Less common but more serious causes include cardiac and central nervous system syncope. Reflex (vasovagal) syncope This is caused by exaggerated but normal cardiovascular reflexes, and so occurs in otherwise healthy individuals, mainly children and young adults. Clinical features Table 1 shows characteristics distinguishing vasovagal syncope from epileptic seizures. Triggers include prolonged standing (school assembly), rising from lying (bathroom at night), hot crowded environments (restaurant), emotional trauma, and pain (doctor’s surgery).
    [Show full text]
  • Evaluation of Patients with Syncope in the Emergency Department: How to Adjust Pharmacological Therapy
    medicina Review Evaluation of Patients with Syncope in the Emergency Department: How to Adjust Pharmacological Therapy Martina Rafanelli *,†, Giuseppe Dario Testa †, Giulia Rivasi and Andrea Ungar Syncope Unit, Geriatric and Intensive Care Unit, University of Florence and Azienda Ospedaliero-Universitaria Careggi, Largo Brambilla 3, 50134 Florence, Italy; [email protected] (G.D.T.); giulia.rivasi@unifi.it (G.R.); aungar@unifi.it (A.U.) * Correspondence: martina.rafanelli@unifi.it; Tel.: +39-055-7949558 or +39-333-6022642 † Contributed equally to the paper. Abstract: The rate of syncope in the Emergency Department ranges between 0.9 and 1.7%. Syncope is mostly related to a underlying reflex or orthostatic mechanism. A bradycardic or a hypotensive phenotype, may be identified. The latter is the most common and could be constitutional or drug induced. Consequently, obtaining an accurate drug history is an important step of the initial assess- ment of syncope. As anti-hypertensive medication might be responsible for orthostatic hypotension, managing hypertension in patients with syncope requires finding an ideal balance between hypoten- sive and cardiovascular risks. The choice of anti-hypertensive molecule as well as the therapeutic regimen and dosage, influences the risk of syncope. Not only could anti-hypertensive drugs have a hypotensive effect but opioids and psychoactive medications may also be involved in the mechanism of syncope. Proper drug management could reduce syncope recurrences and their consequences. Citation: Rafanelli, M.; Testa, G.D.; Keywords: syncope; orthostatic hypotension; hypotensive phenotype; hypotensive susceptibility; Rivasi, G.; Ungar, A. Evaluation of pharmacological therapy; drugs Patients with Syncope in the Emergency Department: How to Adjust Pharmacological Therapy.
    [Show full text]
  • Syncope: Diagnosis and Treatment – Marc Kraus
    SYNCOPE: DIAGNOSIS AND TREATMENT – MARC KRAUS INTRODUCTION Syncope is a sudden loss of consciousness associated with loss of postural tone (collapse) from which recovery is spontaneous. Pre-syncope is a term used to describe episodic rear-limb or generalized weakness, ataxia, or altered (but not complete loss) of consciousness. The common denominator leading to all forms of syncope is decreased or brief cessation of cerebral blood flow. Severe heart rhythm disturbances are probably the most common causes of syncope in dogs and cats. SYNCOPE OR SEIZURE? Distinguishing syncope from seizure can be difficult. Clues for differential diagnosis include situational triggers, prodromal signs, and behavior during the episode, and the events that follow (Table I). Collapse episodes that are precipitated by exercise, stress, cough, gag, emesis, micturition, defecation, and pain are most likely syncope rather than seizure. Disorientation after the event with slow recovery of normal consciousness is common with seizure. However, protracted cerebral hypoxia resulting from cardiac arrhythmia may also be followed by relatively slow recovery. Differentiating seizure from syncope can be confounded by the possibility of “hypoxic convulsive syncope” where prolonged cerebral hypoperfusion results from profound cardiac arrhythmia. Syncope without prodromal signs, without violent tonic-clonic activity, and quick recovery suggests a heart rhythm disturbance. Although usually associated with flaccid collapse, syncope due to arrhythmia can be associated with extensor rigidity and spontaneous urination or defecation. Hypersalivation is rarely associated with syncope due to heart rhythm disturbances. Other causes of transient loss of consciousness include syncope-like episodes caused by hypoxemia or hypoglycemia. WHAT IS NEURALLY-MEDIATED SYNCOPE? The definition of neurally mediated syncope (NMS) is: The development of arterial vasodilatation in the setting of relative or absolute bradycardia.
    [Show full text]
  • Syncope: Evaluation of the Weak and Dizzy
    Syncope: Evaluation of the Weak and Dizzy William M. Miles, MD, FACC, FHRS Professor of Medicine Silverstein Chair for Cardiovascular Education University of Florida College of Medicine Disclosures • Medtronic, Inc. (Clinical Events Committee, consultant) • Biosense-Webster, Boston Scientific, Medtronic, St. Jude (UF EP Fellowship Support) Syncope Is Nothing New William Shakespeare (~1564-1616) Works in Which a Character Faints from Strong Emotion Heaton KW. BMJ 2006; 333:1335 Syncope and Current Events Etiologies of true syncope include: 1. Seizures 2. Trip and Falls 3. Vasovagal faints 4. Intoxications 5. Psychogenic Etiologies of true syncope include: 1. Seizures 2. Trip and Falls 3. Vasovagal faints 4. Intoxications 5. Psychogenic Heart Rhythm, Vol 12, NO 5, June 2015, e41-63 Definition of Syncope Transient loss of consciousness, associated with an inability to maintain postural tone, rapid and spontaneous recovery, and the absence of clinical features specific for another form of transient loss of consciousness such as epileptic seizure 2015 Heart Rhythm Society Expert Consensus Statement on the Diagnosis and Treatment of Postural Tachycardia Syndrome, Inappropriate Sinus Tachycardia, and Vasovagal Syncope Epidemiology of Syncope First faint peak age (15 yo ) a.) First episode typically occurs between ages 10 to 30 b.) Cumulative incidence Increase with age European Heart Journal (2009) 30. 2631-2671 Brignole, M. Heart 2007;93:130-136 Syncope Evaluation European Heart Journal (2009) 30. 2631-2671 Syncope patients with the poorest prognosis are those with: 1. Vasovagal syncope 2. Orthostatic syncope 3. Carotid sinus hypersensitivity 4. Cardiac cause of syncope 5. Syncope of undetermined cause Syncope patients with the poorest prognosis are those with: 1.
    [Show full text]
  • Syncope in Athletes
    Sabatino 1 FLORIDA SOUTHERN COLLEGE Syncope in Athletes Samantha Sabatino 86 Argon Place New Hyde Park, NY 11040 Cell: 516-805-5086 House: 516-248-6631 Email: [email protected] 2010 Winner, Literature Review National Athletic Trainers Association Deloss Brubaker Undergraduate Student Writing Contest Faculty: James M. Lynch, MD Athletic Training Sabatino 2 Abstract Syncope is defined as the transient loss of consciousness with an inability to maintain postural tone followed by a spontaneous recovery. Syncope is a frequently encountered problem with etiologies ranging from benign to life threatening. It accounts for approximately 3% of emergency department visits and between 1 and 6% of acute hospital medical admissions. Syncope is an underlying symptom of a number of different medical conditions. The etiologies can be categorized as cardiac, metabolic, psychiatric, or neurological. The most frequent diagnosis category is cardiac. Cardiac causes of syncope can further be subdivided into the following categories: structural disease, cardiac arrhythmias, neurocardiogenic syncope, carotid sinus syncope, or orthostatic (postural) syncope. When a patient has experienced syncope, a thorough assessment explores associated symptoms, physical examination, environment, drugs, and family history The most commonly used tests for syncope include electrocardiogram (ECG), kidney function tests, table tilt test, carotid sinus massage, and exercise testing. Immediate treatment includes evaluating the individual’s airway, breathing, and circulation (ABC) status and determining if emergency medical help is necessary. Secondary treatment of syncope includes education, maneuvers to avert episodes, drug therapy, and pacemakers. With regard to prognosis associated with syncope, two important elements should be considered: (1) risk of death and life-threatening events; and (2) risk of reoccurrence of syncope resulting in physical injury.
    [Show full text]
  • Increasing Prevalence of Orthostatic Hypotension As a Cause of Syncope with Advancing Age and Multimorbidity
    JAMDA xxx (2019) 1e3 JAMDA journal homepage: www.jamda.com Editorial Increasing Prevalence of Orthostatic Hypotension as a Cause of Syncope With Advancing Age and Multimorbidity Alice Ceccofiglio MD a, Chiara Mussi MD, PhD b, Martina Rafanelli MD, PhD a, Giulia Rivasi MD a, Mario Bo MD, PhD c, Enrico Mossello MD, PhD a, Anna Maria Martone MD d, Pasquale Abete MD, PhD e, Andrea Ungar MD, PhD a,* a Department of Geriatrics, Azienda Ospedaliero-Universitaria Careggi and University of Florence, Italy b Centro di Valutazione e Ricerca Gerontologica, Chair of Geriatrics, University of Modena and Reggio Emilia, Modena, Italy c Section of Geriatrics, Department of Medical Sciences, Città della Salute e della Scienza-Molinette, Torino, Italy d Department of Geriatrics, Neurosciences and Orthopedics, Catholic University of the Sacred Heart, Rome, Italy e Department of Translational Medical Sciences, University of Naples, Federico II, Naples, Italy During recent years, syncope studies have included an situational syncope, and carotid sinus syndrome) was more common e increasing number of older subjects with multimorbidity.1 4 More- in younger patients (z60% vs z35%), whereas orthostatic syncope, over, increasing awareness of pathophysiology today allows a more including drug-induced forms, was more frequent in older ones accurate differential diagnosis of this condition.5 Yet how syncope (z35% vs z10%).2 etiology changes with advancing age and increasing multimorbidity is The “Syncope and Dementia (SYD) registry” was published in still unclear. The present paper thus aimed at comparing and discus- 2016 and was the first study investigating syncope etiology in older sing the results of 3 multicentre studies, and analysing how syncope patients with dementia.
    [Show full text]
  • Autonomic Function in Adolescents with Orthostatic Dysregulation Measured by Heart Rate Variability
    601 Hypertens Res Vol.30 (2007) No.7 p.601-605 Original Article Autonomic Function in Adolescents with Orthostatic Dysregulation Measured by Heart Rate Variability Yuko SATO1), Ko ICHIHASHI1), Yutaka KIKUCHI1), Hirohiko SHIRAISHI1), and Mariko Y. MOMOI1) We evaluated the responses of autonomic nervous system to transient positional changes and daily changes in orthostatic dysregulation (OD) patients in order to clarify the mechanisms underlying the appear- ance of symptoms. The control group consisted of 16 healthy adolescents (8 males and 8 females), and the OD group consisted of 25 adolescents (13 males and 12 females). Each subject underwent continuous elec- trocardiographic monitoring during the head-up tilt test, followed by electrocardiographic monitoring for 24 h. Low frequency power (LF) and high frequency power (HF) were calculated as indices of autonomic func- tion. During 0–5 min in the standing position in the tilt test, HF was higher in the OD group than in the con- trol group (180±110 ms2 vs. 42.6±54.1 ms2; p<0.05). The LF/HF ratio during standing for 15–20 min was higher in OD patients than in the controls (4.75±3.45 vs. 1.67±1.21; p<0.05). The 24 h analysis showed that HF during sleep was significantly lower in the OD patients than in the controls (516±290 ms2 vs. 1,290±429 ms2; p<0.05); the LF/HF ratios were consistently higher in the OD patients than in the controls (4.13±3.41 and 2.92±2.00 vs. 2.46±0.89 and 1.35±1.54 in waking and sleeping states, respectively; p<0.05).
    [Show full text]
  • Adolescent Syncope
    Adolescent Syncope Brett Goudie, M.D. Pediatric Cardiology Syncope • From the Greek word synkoptein, which means “to cut short” • Syncope – “temporary loss of consciousness and postural tone resulting from an abrupt, transient, and diffuse cerebral dysfunction (hypoperfusion), and followed by spontaneous recovery” – cerebral blood flow ↓ 30-50% • Syncopized???? Syncopated? • Pre-syncopize? Syncopal • Pre-syncope – prodromal dizziness and lightheadedness that precedes LOC – aka near-syncope • Sadly I have no financial disclosures related to this topic Syncope – why talk about it? • Common - 15-25% of children experience at least one episode (peak ages 15-19) ♀ > ♂ • Expensive clinical problem / testing / Up to 3 % of ER visits / treatable • Most typically totally benign • 80-90% is vasodepressor (vs cardioinhibitory) ANGST!!!!!!! • Only 1% of time due to arrhythmia or structural cardiac disease / sudden death 1 Vasovagal Syncope Terminology • Vasodepressor (Vaso) • Cardioinhibitory (Vagal) • Neurocardiogenic • POTS – postural orthostatic tachycardia syndrome • Orthostatic Hypotension or Intolerance • Situational • Reflex • Neurally mediated Bryan Cannon, Philip Wackel Pediatrics in Review Apr 2016, 37 (4) 159-168 2 “Fainting Goat” Myotonia Congenita 3 Syncope, at the Carotid Sinus • Upright posture, 25% of blood redistributed to lower extremities • Preload diminished, leads to diminished stroke volume by as much as 40%, CO = HR * SV • Baroreceptors activated (Carotid sinus) • Increased sympathetic activity increases HR, contractility,
    [Show full text]