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Arrhythmias Valerie Seabaugh MD Jerry L Pettis Memorial VA Hospital Today’s discussion Normal ECG components Normal wave conduction physiology Bradycardia Tachycardia Pacemakers and Automatic internal cardiac defibrillators (AICD) Normal ECG By convention, electrical pulses conducted toward the ECG lead are positive those conducted away are negative The P wave Represents atrial depolarization Duration is measure of time required for depolarization to spread through the atria to the AV node Is usually upright in I, II, and aVF Negative in aVR variable in III, aVL The PR interval Represents time required for a supraventricular impulse to depolarize the atria, traverse the AV node, and enter the ventricle Normal is 0.12 to 0.20 seconds, greater than 0.20 is considered first degree AV block The QRS complex Represents ventricular depolarization Q wave – first negative deflection R wave – first positive deflection after a P wave S wave – negative deflection following an R wave Normal is between 0.06 and 0.10 sec The ST segment The isoelectric segment following depolarization and preceding ventricular repolarization From the end repolarization of the QRS to the beginning of the T wave In contrast to PR and QRS intervals, the ST segment length can be variable Elevation or depression of the ST segment by 0.1 mV from the baseline is abnormal The T wave Represents ventricular repolarization T wave vector normally “tracks” with the QRS vector. If QRS is predominantly negative an inverted T wave is not necessarily abnormal The QT interval From the beginning of the QRS complex to the end of the T wave Represents electrical systole Is usually <0.425 seconds duration when corrected for heart rate (QTc = corrected QT interval) Membrane potential in the ventricle, atria, and Purkinje system Phase 0 – Na+ enters the cell Phase 1 – initial repolarization by K+ moving out of the cell Phase 2 – plateau of action potential caused by Ca++ moving into cell Stoelting p 69 Membrane potential in the ventricle, atria, and Purkinje system Phase 3 – Ca++ conductance decreases but K+ conductance increases with K+ moving out of cell Phase 4 – K+ moving out returns cell to resting potential This differs in the SA node where influx of Ca++ starts action potential Effect of electrolyte disturbance on cardiac rhythm Effect of electrolyte disturbance on cardiac rhythm Hypocalcemia – prolonged QT interval, ST segment, V Tach, Torsades Hypercalcemia – shortened QT interval Hypomagnesemia – widened QRS, cardiac irritability Bradycardia – Disturbances of cardiac impulse conduction First degree AV heart block Second degree Mobitz I Mobitz II Unifasicular block R bundle branch block L bundle branch block Third degree (trifascicular ) heart block Defined as HR less than 60 First degree AV block Think of ischemia if it is a new onset for the pt. Can also be caused from digitalis, aortic regurgitation, increased vagal tone Usually asymptomatic 2nd degree AV block Mobitz I (Wenckeback) progressive prolongtion of PR until a beat is entirely blocked 2nd degree AV block Mobitz II Sudden interruption of the conduction of an impulse without prior prolongation of the PR 2nd degree AV block Mobitz II More serious than Mobitz I because it is more likely to progress to complete heart block More likely to require pacemaker “Missing a beat without warning is TWICE as scary” Right bundle branch block Conduction block over the R bundle branch which is present in 1% of hospital patients May be seen in pts with pulm dz, ASD, or increased R ventricular pressures Often clinically insignificant Right bundle branch block QRS complex exceeds 0.1 second Broad rSR complex in V1 an V3 L bundle branch block Often associated with ischemic heart disease, LVH/chronic HTN, or valve disease Difficult to diagnose MI in the presence of LBBB L bundle branch block QRS complex more than 0.12 seconds with wide notched R waves in all leads Unifascicular block 3 fascicles of the His-Perkinje system Right fascicle, Left anterior fascicle, Left posterior fascicle A block of one of the L fascicles can occur One of the L fascicles plus RBBB can lead to complete heart block Complete heart block Complete absence of conduction of impulse from atria to ventricle If block is proximal to AV node HR will be 4555 BPM If block is distal to AV node (infranodal) HR will be 30-40 BPM with a wide QRS (ventricular in origin) Can be caused by fibrotic degeneration, ischemia, cardiomyopathy, ankylosing spondylitis, iatrogenic (cardiac surgery), drugs, hyperkalemia TX is pacing Bradycardia 1001 Differential dxs for bradycardia including: Hypovolemia, hypoxia, acidosis, hypoglycemia, hypothermia, hyperkalemia, overdose, tension pneumo, increased ICP, pesticide exposure, noxious surgical stimulation (ocular pressure, scrotal/ovarian traction, abd insufflation, laryngoscopy), PE, MI, carotid sinus stimulation, narcotics, succinylcholine, sleep apnea, normal physiology of well-trained athlete, hypothyroidism . . . etc Tachycardia (Heart rate greater than 100) Three key questions: IS THE PATIENT STABLE? Is the QRS narrow or wide? Is the rhythm regular or irregular? Tachycardia Narrow complex Regular rhythm is probably a reentrant tachycardia Irregular rhythm is probably A fib or A flutter Wide complex Regular rhythm could be SVT with aberrant waveform or VT Irregular rhythm could be A fib with aberrant waveform, polymorphic V tach, torsades Narrow versus wide complex tachycardia Narrow complex more likely from an atrial origin Aka SVT (supraventricular tachycardia) Wide complex more likely from a ventricular origin VT more serious since the concern is that the rhythm may degrade to V Fib Narrow complex tachycardia Sinus tachycardia Most common cause of tachycardia Rhythm originates from AV node in response to stress Hypovolemia Pain Fever Exercise Substance withdrawl Agitation (in the ICU) . . . etc Treatment is to identify and treat the stressor (if necessary) Narrow complex tachycardia Supraventricular tachycardia SVT can be loosely defined in 3 types Atrial tachycardia-AV node passively conducts impulse from atria to ventricles • A fib, A flutter, atrial tachycardia Atrioventricular nodal reentrant tachycardiareentrant focus is adjacent to AV node and AV node propogates reentrant impulse AV reentrant tachycardia-accessory pathway bypasses the AV node • WPW Narrow complex tachycardia Supraventricular tachycardia Atrial tachycardia Ectopic atrial focus (outside the atrial node) becomes irritable and can override atrial rhythm • See P waves of different morphology Narrow complex tachycardia Atrial fibrillation with RVR Atrial depolarization rate is 400 – 600/minute AV node acts as gatekeeper and only conducts 100-180 of these depolarizations each minute Atrial Flutter Atrial depolarization rate is 250450/minute Narrow complex tachycardia A fib/A flutter A Fib A flutter Narrow complex tachycardia A fib/A flutter Treatment If patient is unstable tx is always cardioversion • 50 J for A flutter, 100-200 for a fib progressing to 200, 300, 360 For stable patients control rate with B blockers, diltiazem, consider amiodorone for new onset Narrow complex tachycardia AVNRT & AVRT Reentry tachycardia requires two pathways over which impulses are conducted at different velocities Can originate adjacent to the AV node Pathway may completely bypass AV node (giving rise to WPW) Narrow complex tachycardia AVNRT & AVRT If the supraventricular tachycardia is due to AV node reentry then it should be terminated by anything that transiently blocks the AV node Carotid massage Valsalva Adenosine Definitive tx is ablation of the accessory pathway Narrow complex tachycardia AVNRT & AVRT Accessory pathway which bypasses AV node poses risk for sudden cardiac death due to tachyarrhythmias WPW syndrome on ECG has delta wave or slurred deflection of beginning of QRS, QRS greater than 0.12 sec Pacemakers and AICDs Chamber paced Chamber sensed Response of generator Prgrammable functions of the generator V = ventricle V = ventricle T = triggered P= programmable rate A = atrium A = atrium I = inhibited M= multi programmable D = dual (atrium and ventricle D = dual D = dual C= communicating O = none O = none O = fixed (asynchrynous) (asynchrynous) function ICD (implantable/internal cardiac defibrillator) For patients with a high risk or personal history of ventricular fibrillation Device delivers a defibrillating shock if V tach or V fib is sensed Things to consider in pacemaker/ICD patients Central venous line placement can displace recently placed transvenous electrodes Grounding pad needs to be placed far away from device If cautery is used near device, current should be as low as possible and delivered in short bursts Things to consider in pacemaker/ICD patients Should defibrillation be necessary in pacemaker patient, paddles should not be placed directly over the pulse generator and patient may have lower stimulation threshold For ICDs it is usually prudent to disable the device since sensing of electrocautery may trigger shock External defibrillator should be readily available and device should be turned on immediately post op THINGS TO REMEMBER Your response to a patients dysrhythmia is dependent on whether the patient is stable or unstable Bradycardia of 45 in an Olympic athlete is acceptable for a BP of 120/80 but not for 60/40 A heart rate of 130 is NORMAL in an infant but could cause an MI for a 78 year old hypertensive, diabetic, smoker You are walking down the hall of the surgical floor when a nurse recognizes that you are on the surgical team and stops you regarding Mr. Brown. He is a 28 y/o that had an appendectomy at midnight last night. His heart rate was 120 when the CNA took his vitals 5 minutes ago. What is your next step? You go to see Mr. Brown. He does not appear to be in pain, but does look pale and anxious. You pick up his wrist and count a thready pulse of 135. His vitals are RR 28, BP 85/65, Temp 100.9 He states he has no heart problems or history of syncope. He runs 2 miles a day. His father died of an MI at 54. On further exam you notice Mr. Brown’s abdomen seems more tender than you would expect. The lab calls with a panic value of Hgb of 5.2 for Mr. Brown You receive a stat page to the ward because Mr. Jones has been found to be lethargic this morning. He is only mumbling incomprensibly when you ask him questions or shake his shoulder. Mr. Jones is a 78 year old that had a total knee replacement yesterday. Vital signs are SpO2 85%, HR 45, RR 6, BP 82/40 Mr. Jones is lying in bed with his mouth hanging open. His eyes are rolled back. He is making course, snoring sounds with his respirations. His dressing looks clean and dry. He has NS for IVF running at 120/hour and a morphine PCA. After oxygen mask is placed his saturation improves to 95% 0.5 mg of atropine improves his heart rate to 85 His mental status improves somewhat but he is still extremely somnalent On further exam Mr. Jones is noted to have a PCA basal dose of 4 mg/hour of morphine. After administering naloxone, Mr. Jones becomes responsive, conversant and begins asking for a breakfast tray