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A SHORT APPROACH TO SUDDEN ONSET SYNCOPE.pptx
- 1. SYNCOPE, other namesFainting, blacking out, passing out, swooning A 1744 oil painting by Pietro Longhi called Fainting
- 2. DEFINITION OF SYNCOPE •Syncope is a self-limiting, transient loss of consciousness caused by inadequate cerebral blood flow that results in inadequate cerebral perfusion. • There is associated loss of postural integrity. • A spontaneous return to baseline levels of neurologic function without the need for resuscitation or intervention is typical. • Presyncope (also known as near-syncope) is part of the syncope spectrum. • Like syncope, it may present with prodromal symptoms. • However, there is no loss of consciousness.
- 3. EPIDEMIOLOGY • Accounts for: –> 2% of all ED encounters – > 5% of all hospital admissions • Lifetime prevalence in general population: approximately 10%–20% • Occurrence has a bimodal age distribution: – A peak in late adolescence to early adulthood (mostly vasovagal origin) – Second peak in older age, with a sharp rise thereafter
- 4. CEREBRAL CIRCULATION The twomain pairs of arteries are the internal carotid arteries (supply the anterior brain) and vertebral arteries (supplying the brainstem and posterior brain). Brain comprises 2% of body-weight but receives 20% share of cardiac output. Normal Cerebral blood flow is 50 – 60 ml/min/100 gm of brain tissue maintained at a Cerebral Perfusion Pressure in the range of 50 – 150 mm Hg. A constant rate of Cerebral blood flow is maintained at varying level of perfusion pressure through an auto regulatory mechanism . Cerebral blood flow below 25ml/min/100 gm of brain tissue causes impairment of consciousness. Cessation of cerebral blood flow for 6 – 8 sec leads to syncopal attack.
- 5. CEREBRAL AUTOREGULATION CBF =MAP – ICP / CVR = DIAMETER MYOGENIC CONTROL : Vascular smooth muscle tone hence diameter is maintained by activation of stretch sensitive calcium channel. NEUROGENIC CONTROL : Vascular smooth muscle tone is maintained by perivascular neuronal secretion of vasoactive neurotransmitter like Ach, NO, serotonin, Neuropeptide-Y. METABOLIC CONTROL : Rise & fall of paCO2 in cerebral circulation causes dilatation & constriction respectively through proton ion mediated mechanism. ENDOTHELIAL : Dilator-NO, Constrictor- TXA2, ET-1 .
- 6. MECHANISM OF SYCOPE Normally,the heart and the CNS provide hemodynamic inputs to the brain stem, which then balances sympathetic and parasympathetic tone to maintain cerebral perfusion. A failure of this mechanism, in the face of physiological stressor, results in a paradoxical withdrawal of sympathetic tone along with simultaneously increased parasympathetic discharge. Vasodilatation and relative hypotension combined with bradycardia lead to poor cerebral perfusion and syncope.
- 7. NEURALLY MEDIATED SYNCOPE(VASOVAGAL) • Most common cause of syncope among young adult. • Caused by a reflex that increases vagal tone and/or decreases sympathetic tone (i.e., excessive autonomic reflex activity) • As a group, referred to as “situational syncope” & include: – Emotional stress: • Witnessing trauma • Sight of needles or blood • Extreme anxiety or panic attack • Extreme pain – Prolonged standing – Micturition – Defecation – Swallowing – Coughing/sneezing – Carotid hypersensitivity: • Syncope (or presyncope) resulting from excessive reflex response to carotid sinus stimulation • Stimuli include head turning, tight neckwear, shaving.
- 8. ORTHOSTATIC HYPOTENSION • Volumedepletion • Hemorrhage: – Traumatic hemorrhage – Retroperitoneal hemorrhage – GI blood loss – Splenic rupture – Obstetric/gynecologic blood loss • GI losses: – Vomiting – Diarrhea • Diminished thirst drive (primarily in older individuals) • Water deprivation • Diuretic use • Immobility/ deconditioning • Autonomic dysfunction • Primary: – Pure autonomic failure – Parkinson disease – Multiple system atrophy – Lewy body dementia • Secondary: – Diabetes mellitus – Amyloidosis – Spinal cord injury – Autoimmune neuropathy – Paraneoplastic neuropathy
- 9. CARDIAC SYNCOPE • Heartrhythm disturbances: – Tachyarrhythmia: • Supraventricular tachycardia • Ventricular tachycardia – Bradyarrhythmias (with inadequate ventricular compensation) • Sinus node dysfunction • Atrioventricular block – Other: • Long QT syndrome • Brugada syndrome • Pacemaker failure • Myocardial ischemia – MI – Ischemic cardiomyopathy – Left ventricular free wall rupture • Structural heart disease: – Hypertrophic cardiomyopathy – Cardiac tamponade – Severe native valve disease: • Mitral valve stenosis • Aortic valve stenosis • Aortic insufficiency – Prosthetic valve dysfunction – Congenital coronary anomalies – Cardiac masses and tumors (e.g., atrial myxoma)
- 10. DRUG RELATED SYNCOPE •Diuretics (e.g., thiazides or loop diuretics – May induce volume depletion – May induce electrolyte disturbances • Vasoactive medications (e.g., calcium channel blockers, beta blockers, alpha blockers, nitrates ) – May induce vasodilatation – May induce bradycardia – or suppress vascular autoregulation • Antiarrhythmics: – May predispose to development of prolonged QT interval – Prolonged QT interval predisposes to torsade de pointes • Antidepressants (e.g., tricyclic drugs, selective serotonin reuptake inhibitors) – Indirect mechanism related to suppression of sympathetic neurotransmitters – May suppress vascular autoregulation
- 11. VASCULAR SYNCOPE CEREBROVASCULAR • Bilateralcarotid artery disease • Subclavian steal syndrome • Global cerebral hypoperfusion • Epidural hematoma (“lucid interval”) • Subarachnoid hemorrhage • Transient ischemic attack GREAT VESSELS PATHOLOGY • Pulmonary embolism ( saddle embolus ) • Severe pulmonary hypertension • Aortic dissection
- 12. TOXIC METABOLIC SYNCOPE •Electrolyte disturbance • Hypoxia • Hypoglycemia • Intoxication: – Alcohol – Illicit drugs – Prescription medication use disorder
- 13. CLINICAL PRESENTATIONS PRESENTING SYMPTOMS •Sudden loss of consciousness & postural tone for a brief moment. • Spontaneous return of consciousness. • Individual may report fatigue or tiredness. • Return of consciousness to the previous neurologic baseline without the need for resuscitation. PRODROMAL SYMPTOMS • Light-headedness • A feeling of being warm or cold • Sweating • Palpitations • Nausea or nonspecific abdominal discomfort • Visual blurring; can proceed to temporary darkening • Diminution of hearing and occurrence of unusual sounds • Pallor reported by onlookers
- 14. RED FLAGS :NEEDED FURTHER EVALUATION • Syncope during exertion • Syncope while supine • Multiple recurrences within a short period of time • Heart murmur or other findings suggesting structural abnormalities • Older age • Significant injury during syncope • Family history of: – Sudden unexplained death – Exertional syncope – Unexplained recurrent syncope – Seizures
- 15. HISTORY • Number, frequency,and duration of episodes • Onset • Position • Trauma sustained during loss of postural tone • Provocative factors: – During or immediately after exertion/exercise (red flag) – During or immediately after: • Micturition • Defecation • Coughing • Swallowing – While in a warm and/or crowded place – During prolonged standing – During the postprandial period – In association with: • Emotional stress • Fear • Intense pain – Immediately following carotid sinus stimulation – While supine (suggestive of a serious problem)
- 16. HISTORY • Associated symptomspreceding and/or following the event: – Nausea – Vomiting – Feeling cold or clammy – Visual auras or blurry vision – Palpitations – Shortness of breath – Chest pain • Additional symptoms following the syncopal event: – Confusion – Fatigue – Injury – Bladder or bowel incontinence – Recurrent syncope
- 17. HISTORY • Witnessed signs: –Manner in which collapse happened – External appearance of individual – Estimated duration of loss of consciousness – Physical movements noted – Any breathing changes seen – Associated trauma
- 18. HISTORY • Preexisting medicalconditions: – Structural heart disease: • Ischemic heart disease • Valvular heart disease • Congenital heart disease • Cardiomyopathies • Prior cardiac surgery – Neurologic conditions: • Seizure disorders • Migraine & headaches • Parkinson disease • Stroke – Diabetes mellitus: • Predisposition to cardiovascular / cerebrovascular disease • Prone to development of autonomic neuropathy – Intoxication: • Alcohol • Illicit drugs • Prescription narcotics (e.g., opioids, benzodiazepines, amphetamines)
- 19. HISTORY • Medications: – Diuretics –Antihypertensive agents – Antiarrhythmic agents • Family history: – Sudden death (< 40 years of age) – Familial cardiomyopathy – Seizure disorders – Migraine & headaches – Familial predisposition to syncope
- 20. PHYSICAL EXAMINATION • Vitalsigns: – Pulse and blood pressure taken with individual supine, seated, and standing (orthostatic vital signs) • Drop of systolic BP > 20 mm Hg diagnostic of orthostatic hypotension • Drop of systolic BP > 30 mm Hg in hypertensive individuals – Note speed and regularity of pulse. – Note rate, regularity, and intensity of breathing effort.
- 21. PHYSICAL EXAMINATION • Cardiacexamination: – Note presence of heart murmur, especially if new or worsened. – Comparative pulse timing and blood pressure: • Incongruence between upper limbs indicative of proximal aortic dissection • Incongruence between upper and lower limbs indicative of distal aortic dissection – Note presence of jugular venous distention (JVD), pulmonary rales, peripheral edema. – Note presence of bruits, especially if new or worsened.
- 22. PHYSICAL EXAMINATION • Neurologicexamination: – Note cognitive status, presence of disorientation, or confusion. – Note level of consciousness, especially if deteriorating. – Note presence of focal neurologic deficit(s).
- 23. INVESTIGATION ECG - isindicated for all individuals presenting with syncope, regardless of suspected etiology. ECG monitoring should be continued throughout the ED or hospital stay. Notable findings may include: • Arrhythmias • ECG changes suggestive of cardiac ischemia • PR segment, QRS duration, QT interval prolongation (especially if new or worsened) • Right heart strain pattern (S1, Q3, T3) suggestive of PE • Conduction blocks • Specific signs of congenital or acquired structural heart disease
- 24. INVESTIGATION • Echocardiography Usedto screen for structural heart disease in known or suspected cases • May detect: – Valvular abnormalities – Wall-motion abnormalities – Left ventricular dysfunction – Elevated pulmonary pressures (suggestive of PE) – Pericardial effusion – Masses – Vegetations
- 25. INVESTIGATION • CBC: – RBCindices for: • Anemia • Blood loss • Erythrocytosis – WBC indices for: • Evidence of infection • Lymphoproliferation – Platelet count for: • Bleeding • Thrombotic tendencies • CMP to evaluate for: – Renal or hepatic dysfunction – Electrolyte disturbance – Acid–base imbalance – Hypoglycemia
- 26. INVESTIGATION • Coagulation studies –PT/PTT to evaluate for coagulopathy – Especially in suspected intracerebral/cerebrovascular or GI hemorrhage • Cardiac biomarkers: – Includes: • MB isoenzyme of creatine • kinase (CKMB) • Cardiac Troponin • Beta Natriuretic peptide – Evaluate for the presence of ischemic heart disease and/or heart failure • Urine toxicology screen • Urine hCG for women of childbearing age
- 27. INVESTIGATION • Neuroimaging • (CT,MRI of head/brain) for: – Suspected intracranial mass – Intracranial hemorrhage – Cerebrovascular accident – Traumatic brain injury • CTA of the chest or ventilation/perfusion (VQ) scan for suspected PE • Carotid Doppler scan for suspected carotid vascular disease • Abdominal CT or ultrasonography to evaluate for: – Splenic rupture – Aortic aneurysm – Intraabdominal and retroperitoneal bleeding • Abdominoplevic ultrasonography to evaluate for ectopic pregnancy or gynecologic sources of hemorrhage • Lower-extremity ultrasonography to evaluate for deep vein thrombosis (DVT) • Specific imaging indicated for evaluation of other suspected etiologies
- 28. INVESTIGATION • Other tests •Tilt-table test: changes in posture from lying to standing to evaluate cause of syncope • Electroencephalography to evaluate for possible seizure • Holter monitoring or loop recording for cardiac rhythm disturbances that manifest during the initial ED visit or hospital stay • Other specific testing indicated for evaluation of other suspected etiologies
- 29. TREATMENT OF PRODROMALSYMPTOMS • This includes physical counter maneuvers, such as: • Leg crossing: simultaneous tensing of leg, abdominal, and buttock muscles • Handgrip: consists of maximum grip on a rubber ball or similar object • Arm tensing: involves gripping one hand with the other while simultaneously abducting both hands
- 30. IMMEDIATE TREATMENT • Assistthe individual to the ground, chair, or stretcher to avoid traumatic injury. • Lay individual supine with legs elevated to help with venous return to the heart and to eventually restore cerebral perfusion. • Assess vital signs (blood pressure, pulse, respiratory rate). • Observe other signs (pallor, diaphoresis, seizure activity). • Get additional assistance.
- 31. RISK ASSESSMENT – Evidenceof structural or ischemic heart disease – History of structural or ischemic heart disease – Older age – Syncope while supine – Syncope during exertion – Palpitations at time of syncope – Chest pain at time of syncope – Dyspnea at time of syncope – Syncope without prodrome – Family history of sudden cardiac death – Association with thunderclap headache – High-risk physical examination findings: • Abnormal vital signs • Abnormal cardiac exam • Abnormal pulmonary exam • Abnormal neurologic exam – Abnormal ECG – Persistently low blood pressure – Low hematocrit
- 32. PROMPTLY RULE OUTLIFE-THREATENING CAUSES OF SYNCOPE OR SYNCOPE MIMICS • MI • Nonperfusing cardiac arrhythmia • PE • Cerebrovascular accident • Intracranial hemorrhage • Aortic rupture • Massive hemorrhage • Seizure
- 33. MEASURES TO PREVENTREFLEX SYNCOPE • Reassurance and education about nature, risks, and prognosis. • Avoid mechanical manipulation of the carotid sinuses (e.g., abrupt turning of the neck, wearing tight collars). • Vasodilators should be avoided or reduced where possible. • Medication: – Midodrine – Beta blockers – Paroxetine – Disopyramide • Pacemakers (those with cardioinhibitory responses)
- 34. MEASURES TO PREVENTORTHOSTATIC HYPOTENSION • Medication-induced: – Discontinue offending medication. – Substitute with an alternative agent. – Adjust dose. – Change timing of drug administration. • Volume depletion: – Volume resuscitation – Discontinue/adjust dose of diuretics. – Counsel about hydration and salt intake. – Treat underlying cause (e.g., gastroenteritis, hemorrhage).
- 35. CAUSES OF SYNCOPETHAT WARRANT IMMEDIATE ADMISSION/INTERVENTION Cardiac emergencies: • Arrhythmias: – Documented, suspected, or induced ventricular tachycardia: • Advanced cardiac life support (ACLS) protocol if indicated • Antiarrhythmics • Catheter ablation • Implantable cardioverter–defibrillator – Supraventricular arrhythmias: • ACLS protocol if indicated • Antiarrhythmics • Catheter ablation – Bradyarrhythmias: permanent pacemakers • Ischemic heart disease (IHD) or acute coronary syndrome (ACS): – Activate ACS protocol if indicated. – Coronary intervention or cardiac surgery if indicated • Obstruction to left ventricular outflow caused by aortic stenosis: – Balloon valvuloplasty – Aortic valve replacement
- 36. CAUSES OF SYNCOPETHAT WARRANT IMMEDIATE ADMISSION/INTERVENTION • Cerebrovascular emergencies: • Immediate noncontrast CT of head if cerebrovascular accident (hemorrhagic or ischemic) or intracranial hemorrhage is suspected • Appropriate admission/transfer/consultation depending on findings: – Neurology – Neurosurgery – Interventional vascular team: • Interventional radiology • Interventional vascular surgery • /neurosurgery – Neurologic ICU monitoring
- 37. CAUSES OF SYNCOPETHAT WARRANT IMMEDIATE ADMISSION/INTERVENTION • Hemorrhagic emergencies: • Hemodynamic stabilization: – Volume resuscitation – Administration of appropriate blood products • Stop/reverse anticoagulation • Appropriate surgical consultation if indicated: – Gastroenterology – Interventional vascular team – Obstetrics/gynecology
- 38. DIFFERENTIAL DIAGNOSIS OFSYNCOPE • Seizure • Cerebrovascular accident • Traumatic brain injury • Intoxication • Conversion disorders • Brain tumor
- 39. POSTERIOR REVERSIBLE ENCEPHALOPATHYSYNDROME (PRES) PRES is a neurological condition characterized by swelling in the posterior part of brain. There are regional differences in autonomic innervations, Sympathetic nerves have a denser presence on the anterior circulation compared with vertebrobasilar arteries and their branches . PRES likely involves a combination of factors, including dysregulated cerebral autoregulation, endothelial dysfunction, blood-brain barrier disruption, and potentially hypertension, leading to vasogenic edema in the posterior brain regions.. PRES can be triggered by various factors, including Severe hypertension, Certain medications like Immunosuppressant, chemotherapeutic agents, Eclampsia , preeclampsia, Autoimmune diseases, Renal failure, Infection. PRES can manifest with a variety of symptoms, including Altered mental status , Seizures , Visual disturbances, Headache , Nausea and vomiting, other neurological deficits. With timely diagnosis and treatment, PRES is usually reversible, and most individuals make a full recovery.
- 40. CEREBRAL AUTOSOMAL DOMINANTARTERIOPATHY WITH SUBCORTICAL INFARCTS AND LEUKOENCEPHALOPATHY (CADASIL) A rare genetic disorder that affects small blood vessels in the brain. It's caused by a mutation in the NOTCH3 gene that causes degeneration of vascular sooth muscle leading to loss of vascular tone causing dysfunction of cerebral autoregulation leading to recurrent micro infarct . The subcortical white matter can be diffusely involved, there is relative sparing of the occipital and orbitofrontal subcortical white matter. Leading to a variety of neurological symptoms, including migraine, stroke, and progressive cognitive decline. While there is no cure, treatment focuses on managing symptoms and reducing the risk of complications.