Syncope Student PDF

SYNCOPE Hillary Hammond DVM, MS, DACVIM (Cardiology)  LEARNING OBJEC TIVES Define syncope and describe its distinguishing features Understand the pathophysiology for why syncope occurs Know differential diagnoses for syncope Develop a plan for diagnostic evaluation of pat...

SYNCOPE Hillary Hammond DVM, MS, DACVIM (Cardiology)  LEARNING OBJEC TIVES Define syncope and describe its distinguishing features Understand the pathophysiology for why syncope occurs Know differential diagnoses for syncope Develop a plan for diagnostic evaluation of patients presenting for syncope  SYNCOPE DEFINED Sudden, transient loss of consciousness associated with loss of postural tone, from which recovery is spontaneous Importance of syncope: May be premonitory sign of a serious cardiac problem Impact on quality of life May lead to injuries Events are distressing to owners Sign of a wide range of conditions Treatment nearly impossible without clear understanding of cause 33-50% of dogs, 25-42% of people with syncope discharged without a diagnosis  SYNCOPE DEFINED Occurs when: Cerebral blood flow is briefly interrupted OR When oxygen or nutrient delivery is impaired for other reasons The main determinant of cerebral blood flow is cerebral perfusion pressure (CPP), which is determined by mean arterial blood pressure (MAP) and by intracranial pressure (ICP): CPP = MAP – ICP Cerebral perfusion pressure can be reduced, and syncope can result from either a decrease in MAP or an increase in ICP.  CPP = MAP - ICP Non-cardiogenic Cardiogenic Neurologic Metabolic Increased intracranial pressure Abrupt decrease in oxygen or (ICP) via nutrient delivery to the brain - Cerebral edema (unrelated to perfusion) MAP - Brain tumors - Inflammation - Decrease in oxygen carrying CO SVR - Vascular obstruction capacity aka anemia - Hypoglycemia Usually occurs gradually and is - More commonly: weakness, persistent → not transient seizures  C ARDIOGENIC (REDUC ED C ARDIAC OUTPUT) Arrhythmias Reduced Structural preload heart disease Bradyarrhythmia Cardiac Cardiomyopathy Tachyarrhythmia Tamponade Hypovolemia Congenital Heart Disease Pulmonary Arterial Valvular heart Hypertension disease Obstructive lesions C ARDIOGENIC SYNCOPE Bradyarrhythmias leading to syncope Pause in rhythm >6-8 seconds = loss of consciousness Fixed, low HR may lead to syncope with exertion Decreased heart rate → decreased stroke volume → decreased CO Most common clinically significant bradyarrhythmias: Sick sinus syndrome 3rd degree atrioventricular block, high grade 2 nd degree Atrial standstill  BRADYARRHYTHMIA Oreo, 10-year-old FS Miniature Schnauzer Presented to ER with recurrent episodes of “falling asleep”  BRADYARRHYTHMIA 2 seconds (HR 30 bpm) 1.38 seconds (HR 43 bpm) Lead II ECG, 25 mm/sec. 2-year-old MC Samoyed Lethargy, exercise-induced collapse Lead II ECG, 50 mm/sec. 7 yo FS pomeranian Lethargy, episodic weakness; Serum K + = 8.3 C ARDIOGENIC SYNCOPE Tachyarrhythmias leading to syncope Severe tachycardia (often >300 bpm) → reduced diastole (inadequate ventricular filling time) → reduced stroke volume → reduced cardiac output Most common clinically significant tachyarrhythmias: Ventricular arrhythmias due to cardiomyopathy Dilated cardiomyopathy (esp. Doberman pinschers) Arrhythmogenic right ventricular cardiomyopathy (Boxers) “aborted sudden death” Supraventricular tachyarrhythmias (incl atrial fibrillation) Less likely to result in sudden death  TAC HYARRHYTHMIA Brutus, 9 year old MN Boxer Owner reports he plays too hard and falls over. BRUTUS’ ELECTROCARDIOGRAM 25 mm/sec, average heart rate - 140 bpm RESULTS OF BRUTUS’ HOLTER MONITOR, DAY 1 RESULTS OF BRUTUS’ HOLTER MONITOR, DAY 2 RESULTS OF BRUTUS’ HOLTER MONITOR C ARDIOGENIC SYNCOPE Reduced preload leading to syncope Ventricular filling is determined by: Venous return Diastolic compliance Ability of ventricles to hold adequate blood volumes Inadequate ventricular filling → decreased stroke volume → decreased CO C ARDIAC TAMPONADE RESU LTING IN REDUC ED PRELOAD Cardiac tamponade in 7 year old MN Golden Retriever  PH RES ULTING IN REDU CED PRELOAD Pulmonary hypertension leads to syncope: Increased pressure in the pulmonary arteries → strain of the right ventricle → decreased CO by impairment of left ventricular filling C ARDIOGENIC SYNCOPE Structural heart disease leading to syncope Structural heart disease as cause of syncope is associated with an increased risk of death Patients usually have exertional syncope: Normal: vasodilation in exercise is countered by an increased cardiac output (CO) Diseased heart: unable to sufficiently augment CO to meet needs CHF patients may have increased risk of syncope due to: Poor cardiac output Hypoxemia Associated arrhythmia Treatment with vasodilatory agents  STRUCTURAL HEART DISEASE: C ARDIOMYOPATHIES Dilated cardiomyopathy Hypertrophic (DCM) cardiomyopathy (HCM) Eccentric hypertrophy + poor Concentric hypertrophy systolic function Reduced LV filling space, reduced Reduced contractility compliance SV CO  STRUCTURAL HEART DISEASE: OBSTRUCTIVE LESIONS LEFT Obstructions RIGHT Obstructions Examples: aortic stenosis, intracardiac Examples: pulmonary valve stenosis, tumors, dynamic outflow heartworm disease, pulmonary obstructions (SAM with HCM) thromboembolism Increase afterload Decrease venous return SV CO  STRUCTU RAL HE ART DISEASE: CO NG ENITAL RIGHT TO LEFT SHUNTING Communication between RIGHT and LEFT sides of the heart combined with an increase in right heart pressures Poorly oxygenated blood to bypass the lungs, desaturating systemic circulation Desaturated hemoglobin (hypoxia) Sludgy blood (polycythemia) Most common: Tetralogy of Fallot, Eisenmenger’s syndrome (reversed PDA, reversed VSD)  CPP = MAP - ICP Non-cardiogenic Cardiogenic Neurologic Metabolic Increased intracranial pressure Abrupt decrease in oxygen or (ICP) via nutrient delivery to the brain - Cerebral edema (unrelated to perfusion) MAP - Brain tumors - Inflammation - Decrease in oxygen carrying CO SVR - Vascular obstruction capacity aka anemia - Hypoglycemia Usually occurs gradually and is - More commonly: weakness, persistent → not transient seizures Neurally-mediated reflexes  NEURALLY-MEDIATED REFLEXES Benign group of conditions in which cardiovascular reflexes respond to a trigger by inappropriately signaling vasodilation and bradycardia, causing a sudden drop in BP 2 “types” recognized in animals: Neurocardiogenic bradycardia (NCB) Triggered by extreme excitement, exercise, emotional stress Boxer dogs predisposed* Situational syncope (“vasovagal syncope”) Triggered by events that increase vagus nerve stimulation Cough syncope (“cough-drop”), micturition syncope, syncope following vomiting, defecation or pulling on a lead NEUROCARIOGENIC SYNCOPE Thomason, et al. “JVIM 2008  Historical findings HOW TO DIAGNOSE Physical examination SYNCOPE Step-wise diagnostic plan  1. HISTORIC AL FINDINGS Syncope v. Seizure May suggest situational syncope or point toward underlying cause Characteristics/length of episode “triggers” – circumstances surrounding the episode Medications  TRANSIENT LOSS OF CONSCIOUSNESS SYNCOPE VS. SEIZURE SYNCOPE SEIZURE Sudden, loss of consciousness associated with loss of Physical manifestations of abnormal, excessive postural tone, from which recovery is spontaneous cerebral electrical activity Transient hypoperfusion (5-20 sec) of portion of Characteristics: brain responsible for consciousness Prodromal symptoms Rhythmic movements, hypersalivation, Characteristics: chomping May be precipitated by certain situations Variable duration (>5 minutes suggests Motionless or extensor rigidity, seizure) opisthotonus, spontaneous Slow return of consciousness, prolonged urination/defecation, “jerking” limbs disorientation Short duration Rapid recovery of normal mentation Also rule out: narcolepsy, cataplexy  SYNCOPE OR SEIZURE? Differentiating between syncope and seizure can be difficult! Convulsive syncope - seizure activity from cerebral hypoperfusion (12-15% of people) 15 seconds: Minutes: Loss of consciousness, pallor, Generalized spasms and Weakness/”pre-syncope” Generalized seizures, shock muscle relaxation incontinence Duration of cerebral anoxia  SYNCOPE OR SEIZURE? Differentiating between syncope and seizure can be difficult! Convulsive syncope - seizure activity from cerebral hypoperfusion (12-15% of people) Complex partial seizures - decreased/lost consciousness, varying degrees of motor activity History can be misleading: Events are distressing - owners may provide exaggerated time estimates The frantic struggle to rise after syncope can be misinterpreted Encouraging owner to take video of episodes can be useful!  2. P HYSIC AL EX AM INAT ION /DIAG NO ST ICS Cardiogenic syncope is of greatest prevalence and confers greatest risk - determine presence of heart disease! Careful physical examination, thoracic auscultation ECG (all cases - even if no arrhythmia heard!) Thoracic radiographs If available, thoracic/abdominal FAST scan - remember pericardial effusion!  3. DIAGNOSTIC PLAN Don’t skip the “easy stuff” (minimum data base) BP measurement PCV/TS, glucose Urine specific gravity Chemistry panel - BUN/creatinine, glucose, potassium levels  3. DIAGNOSTIC PLAN CONT’D 24-hour ambulatory ECG (Holter monitor) lennychapman.JPG If an underlying cause is not identified, additional diagnostics should be pursued in: Breeds at high risk for sudden death due to arrhythmogenic cardiomyopathy: Boxer dogs (ARVC), Doberman pinschers (DCM) Breeds predisposed to tachy/bradyarrhythmia: Labrador retrievers (SVT); Schnauzers, WHWT, Cocker spaniels (SSS) Syncope with exertion/exercise Episodes of increasing frequency Dogs who do not return to normal between episodes Echocardiography  TAKE HOME POINTS Syncope is a sudden temporary loss of consciousness that can be caused by cardiac disorders, hypotensive and reflex vagal syndromes, neurologic disease, or metabolic abnormalities. Cardiac disease results in syncope because of decreased CO and blood pressure with a resultant decrease in cerebral perfusion pressure. Cardiac syncope is often associated with stress or exertion because the compromised heart cannot increase CO adequately to meet the increased oxygen demand. Because CO is determined by heart rate (HR), contractility, ventricular filling, and afterload, diseases that affect these parameters may result in syncopal episodes. Diagnosing syncope can be challenging. A detailed history is a crucial when trying to differentiate syncope from other similar episodes. A thorough history, physical examination, and initial database consisting of a complete blood count, chemistry profile, urinalysis, electrolytes, blood pressure, and ECG are important in developing an accurate differential list. CASE PRACTICE 12 YR OLD FS CKC S 5 YR OLD MALE CHIHUAHUA MIX 2 YR OLD FEMALE GOAT  QUESTIONS? Email: [email protected]