CARDIAC DYSRHYTHMIAS Listen to Audio General Pathophysiology Four general causes Evaluating Dysrhythmias Supraventricular Dysrhythmias Ventricular Dysrhythmias general cardiac dysrhythmias may be: -asymtomatic -symptomatic (syncope, new syncope, dizziness, fatigue, palpitations) -lethal ( sudden cardiac death) consequence of dysrhythmias is determined by the extent it reduces the cardiac output therfore perfusion to the brain and heart SVT: -generally well tolerated if no history of heart disease -may lead to myocardial ischemia or heart failure in patients with cardiac history (ex.CAD, valvular heart disease, systolic dysfun.) VT: -if greater than 10-30 seconds often leads to hemodynamic instability and may lead to ventricular fibrilation pathophysiology Possible causes: -genetic abnormalities (ex. affecting ion channels) -acquired structural heart disease -electrolyte abnormalities -hormonal imbalances (ex. thyrotoxicosis, hypercatecholamine states) -hypoxia -drug effects (ex. QT prolongation changes in automaticity, conduction or refractiveness) -myocardial ischemia four general causes of dysrhythmias Automaticity (conduction formation) responsible for: -sinus node arrest -premature beats -automatic rhythms -initating factor in re-entry circuits Impulse conduction responsible for: may occur in: -SA exit block -SA or AV node -AV block at the node or below -intraventricular conduction system -establishing re-entry circuits -within the atria or ventricle Re-entry responsible for: -premature beats -paroxysmal SVT -atrial flutter -infarct related ventricular tachy must have an area of unidirectional block with an appropriate delay allows for repolarization for the repeat depolarization at the site of origin Triggered activity Two Categories -pause dependant: caused by early afterdepolarization in phase 3 in action potentials ventricular tachycardia is typically polymorphic -catecholamine dep: caused by late afterdepolarization in phase 4 in action potentials evaluating dysrhythmias ecg monitoring heart rate variability signal averaged ecg electrophysiologic testing autonomic testing ECG MONITORING patients with recent/recurrent syncope or aborted sudden cardiac death are often monitored in the hospital -patients with infrequent episodes preferably have event recorders (implantable or external) compared to a 24hr continous monitor -patients with symptoms associated with exertion have an exercise tolerance test -patients with less omnious symptoms may possibly be monitored as an outpatient -patients with symptomatic bradycardia or symp. SVT may usually be started on therapy without additional diagnostic studies HEART RATE VARIABILITY -measurements are generally made in controlled conditions in the ecg lab and from recordings from ambulatory monitoring -greater fluctuations are associated with greater parasympathetic activity -studies suggest better prognosis and fewer life threatening dysrhythmias with a greater parasympathetic activty -RR cycle length variability may provide: -indices of the relative balance between the parasympathetic and sympathetic systems -help in determination of the prognosis in patients with postinfarction injury and symptomatic dysrhythmias ex. patients with CHF and decreased HR variability may be associated with worse outcomes SIGNAL AVERAGED ECG ex.orthagnal three lead system -records 300 consecutive beats during basal conditions "late potentials" -are identified in the period following the QRS complex -very low frequency signals detected using a filter and computer averaging of the signals Presense of late potentials may be: -considered markers for potential ventricular dysrhythmias -useful in detecting groups of patients at increased risk for dysrhythmic events S/P MI ex. 1/3 patients S/P MI: -will have abnormal late potentials -may be at higher risk for dysrhythmic events -association has a relatively low positive predictive value of approximately 10 -15% Absense of late potentials: -may indicate low risk for dysrhythmic events ex. post MI patients (with frequent ventricular ectopy or nonsustained Vtach) with absense of late potentials: -may not require further investigation -may not require further treatment ELECTROPHYSIOLOGIC TESTING -intracardial ECG recordings -programmed atrial and/or ventricular stimulations General -used to diagnose and manage complex dysrhythmias Primary indications: -evaluation of recurrent syncope of possible cardiac origin especially when the ambulatory ecg has not provided aspecific diagnosis -differentiation between SVT and VT -evaluate therapy in patients with accessory atrioventricular pathways -evaulate patients for cardiac ablation procedure or antidysrhythmic devices AUTONOMIC TESTING/ TILT TABLE TESTING -helps differentiate between cardiac and neurocardiogenic origin of recurrent syncope or near syncope Neurocardiogenic origin associated with: -excessive vagal stimuli -imbalance between the sympathetic and the parasympathetic nervous system ex. from the supine to upright position: -there is an increase in venous pooling (decreased preload due to increased venous capacitance) -normal compensatory response is increased sympathetic mediated increase in heart rate, contractility and vasoconstriction -abnormal compensatory response is excessive vagal stimulation -initial decrease in blood pressure stimulates the sympathetic mediated increase in heart rate,contractility and vasoconstriction -the increased MAP stimulates the baroreceptors which in turn excessively stimulates the parasympathetic tone via the vagus n. -the excessive vagal tone provides a reflex bradycardia associated with vasodilation and a possible cause of syncope Tilt table test: -several different protocols -passive tilting the head down at least 70 degrees for approximately 10 -40 minutes + isoproternol infusion -then assume the head up position -approximately 1/3 of the patients with recurrent syncope occur because of bradycardia +/- hypotension patients with carotid sinus hypersensitivity:carotid sinus massage may casue sinus node arrest or AV block Supraventricular Dysrhythmias sinus arhythmia sinus bradycardia sinus tachycardia premature atrial contraction paroxysmal supraventricular tachycardia mutifocal atrial tachycardia atrioventricular junctional rhythms SINUS ARHYTHMIA -cyclic changes in heart rate in association with respiration -increased heart rate with inspiration -decreased heart rate with expiration -due to vagal influence on the normal pacemaker of the heart -no clinical significance -common in both young and elderly SINUS BRADYCARDIA -heart rate < 50 bpm -due to increased vagal influence on the pacemaker of the heart -heart rate usually increases with exercise or atropine -in healthy individuals with sinus bradycardia may be a normal finding -in elderly patients or patients with cardiac disease may indicate sinus node pathology -may be associated with signs of symptoms ex. decreased cerebral perfusion may lead to weakness. confusion and syncope -symptomatic bradycardia may need therapuetic pacing SINUS TACHYCARDIA -heart rate > 100bpm -onset/termination: usually gradual -caused by rapid impulse formation from a normal pacemaker causes: -fever -exercise -emotion -pain -anemia -heart failure -shock -thyrotoxicosis -response to drugs PREMATURE ATRIAL CONTRACTIONS -ectopic focus in the atria which fires before the next sinus node impulse ex. re-entry circuit p-wave usually different in contour than the normal p wave of a sinus node QRS complex abberant QRS complex (wide and bizzare) may occur RR cycle length usually unchanged or slightly prolonged increased heart rate usually abolishes most premature beats PAROXYSMAL SUPRAVENTRICULAR TACHYCARDIA -atrial filbrillation -atrial flutter -wolk-parkinson-white syndrome -avnrt -avrt MULTIFOCAL ATRIAL TACHYCARDIA ATRIOVENTRICULAR JUNCTIONAL RHYTHMS Ventricular Dysrhythmias -pulseless ventricular tachycardia -ventricular fibrillation