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Transcript
Amy Gutman MD ~ EMS Medical Director [email protected] / www.TEAEMS.com Part I: Cardiac Anatomy Review Part II: The Cardiac Cycle Part III: From One Beat to Many Part IV: Rhythm Analysis What is an EKG really looking at? German “Elektrokardiogramm” Record of the heart’s electrical depolarizations & repolarizations over time Arrhythmias, ischemia, & conduction abnormalities Electrolyte disturbances Non-cardiac diseases (i.e. hypothermia, PE) 3 lead “overview” image of heart I (lateral) II (inferior) III (inferior) Useful for checking arrhythmias Not great for looking for ischemic changes Leads I, II & III are “limb leads” Leads aVR, aVL, & aVF are “augmented” limb leads V1 - 4th ICS to right of sternum V2 - 4th ICS to left of sternum V3 - Between V2 & V4 V4 - 5th ICS at MCL V5 - Horizontally with V4 at AAL V6 - Horizontally with V4 & V5 at MAL I AvR V1 V3 II AvL V2 V4 III AvF V3 V5 Lead II Continuous Strip I AvR Lateral V1 Septal V4 Anterior II AvL V2 V5 Inferior Lateral Septal Lateral III AvF V3 V6 Inferior Inferior Anterior Lateral Right Coronary Artery (RCA) perfuses right ventricle / inferior heart Inferior heart Left Main Artery (LMA) divides into: Left Anterior Descending Artery (LAD) perfuses anterior left ventricle Left Circumflex Artery (LCX) perfuses lateral left ventricle Each coronary artery = one part of the EKG You must see changes in >two “contiguous” leads to diagnose ischemia Contiguous leads = heart “territories”: Inferior, Anterior, Lateral, Septal Right ventricle positioned downward & inferior Innervated by vagus nerve Same nerve as stomach IMIs often present with N/V not “chest pain” II Inferior III AvF Inferior Inferior Two vessels cover large area V2 overlaps septal & anterior areas Septal MI is best seen in V1 & V2 V1 Septal V2 Septal Septum & anterior left ventricle are the “precordial” leads V1 & V2 directly over cardiac septum V2 (septal overlap), V3, V4 look at anterior heart V4 Anterior V3 Anterior Winds around lateral heart & left ventricle LMA “Widow Maker”: Divides into LAD & LCX, perfuses left ventricle LMA occlusion causes massive antero-lateral MI I Lateral AvL V5 Lateral Lateral V6 Lateral Contiguous Leads I, AvL, V5, V6 II, III, AvF V1, V2 (V2, V3) V3, V4 I AvR V1 V4 Lateral Septal Anterior LMA, LCX RCA, LAD LAD II AvL V2 V5 Inferior Lateral Septal Lateral RCA LMA, LCX RCA, LAD LMA, LCX III AvF V3 V6 Inferior Inferior Anterior Lateral RCA RCA LAD LMA, LCX The heart is nothing more than a mechanical pump running on electricity The heart is a mechanical pump running on electrical energy Electrical energy pathways determine how well the heart functions Changes in electricity = changes in heart function Left Atrium Sinoatrial Node Atrioventricular Node Bundle of His Right Atrium Right Ventricle Left Ventricle Electrical Pathway SA Node AV Node 1. SA Node 2. AV Node 3. Bundle of His 4. Right & Left Ventricles Right Ventricle His Bundle Left Ventricle One complex = one cardiac cycle Recognizing normal means understanding abnormal Atrial Depolarization Ventricular Depolarization Ventricular Repolarization Width = time Height & depth = voltage Upward deflection = positive Downward delection = negative SA to AV node path causes atrial contraction Upright in II, III, & aVF Inverted in aVR Variable P wave shapes suggests ectopic pacemaker 120 - 200 ms (3 to 5 small boxes) Long = 1st degree heart block Short = pre-excitation syndrome (WPW) Variable = other heart blocks PR depression = atrial injury or pericarditis Short PR interval <120 ms, <3 small boxes Slurred QRS upstroke = “delta wave” Young, healthy person with CP & palpitations Consider with “shackalitis” Atrial impulses conducted to ventricles via accessory pathway causing reentry Ventricular contraction coordinated by Bundle of His & Purkinje fibers 0.06 to 0.10 sec Duration, height & shape diagnose arrhythmias, conduction abnormalities, hypertrophy, infarction, electrolyte derangements Short: <0.08 secs Seen in SVT Long: >0.12 secs Often related to a bundle branch block Normal (physiologic) or abnormal (pathologic) Normal: Septal depolarization Best seen in lateral leads I, aVL, V5 & V6 Qs > 1/3 R wave height, or >0.04 sec length abnormal May show infarction J Point 0.08 - 0.12 sec J point to beginning of T wave Flat or depressed ST: Ischemia ST elevation: Infarction Ventricular repolarization T wave usually upright Inverted: ischemia, hypertrophy, CVA Tall: hyperkalemia Flat: ischemia, hypokalemia Beginning of QRS to end of T wave Ventricular depolarization to “resetting” the conduction system Normal ~ 0.40 secs Interval varies based on HR & must be adjusted (Corrected QT / QTc) • The heart takes too long to repolarize leaving it vulnerable to aberrant electrical impulses • Torsades de pointes, VT, VF Prolonged QT interval Alcohol abuse Hypomagnesemia, hypokalemia May have a pulse, but are never “stable” RX: magnesium bolus Not always seen, typically small, follows T wave Purkinje fiber repolarization Hypokalemia, hypercalcemia, hypothermia, CVA, or thyroid disease Inverted U wave: ischemia, volume overload Putting it together… 1 small block = 1 mm² = 0.04 s = 40 ms 5 small blocks = 1 large block = 0.20 s = 200 ms 5 large blocks = 1 second Each large black line = 300 150 100 75 60 50 If there is an P wave before each QRS & both are upright, then the rhythm is “sinus” From sino-atrial / SA node P wave round, not peaked & unidirectional except in V1 & V2 (often biphasic) Normal axis leads I & AVF are positive (upright) When heart enlarges / hypertrophies or normal pathways are re-routed, the “axis” changes Anything more beyond the scope of this lecture Right Ventricular Hypertrophy R wave >S in V1, becomes progressively smaller S wave in V5,V6 RAD with wide QRS Left Ventricular Hypertrophy S in V1 + R in V5 (in mm) = 35mm LA with wide QRS Why is this important for prehospital providers? Anywhere in conduction system Ectopic beats generated from foci other than usual sites of electrical activity Some ectopic beats in a healthy persons normal Persistent ectopic beats become “blocks” / conduction dz Conduction disorders manifest as slowed conduction (1st degree), intermittent conduction failure (2nd degree), or complete conduction failure (3rd degree) Slowed electrical signal not travelling through atrial tissue at normal speed resulting in long P-R PR > 0.20 sec Always a P waves before QRS P-R interval consistent May be due to ischemia or infarct Progressive delay AV conduction, until impulse completely blocked Occurs because impulse arrives during absolute refractory period, so no conduction no QRS P-P intervals shorten until pause occurs Next P wave occurs & the cycle begins again P-P interval following pause greater than P-P interval before pause Block usually located in AV node, so QRS narrow Multiple constant PR intervals before blocked P wave Ventricular rate always les than atrial rate, depends on number of impulses conducted through AV node Atrial & ventricular rates irregular P waves present in 2, 3 or 4:1 conduction with QRS PR interval constant for each P wave prior to QRS Type II AV block is almost always located in bundle branches so QRS is wide Atria & ventricles controlled by separate pacemakers Narrow QRS suggests AV block with junctional escape Wide QRS suggests AV node or bundle branch block block with ventricular escape (“idioventricular”) •40 – 60 BPM •“Junction” between atria & ventricles •P wave “flipped” as beat originates below SA node LBBB • RBBB • QRS >0.12 • “M” shaped QRS in V1 or V2 • R = 1st peak • Ischemia, infarction, electrolyte abnormalities, meds, CNS disease LBBB QRS >0.1-0.12s • Wide & “Peaked” QRS in V6 • R Prime = 2nd peak Stage I: Ischemia Stage 2: Injury Stage 3: Infarction Stage 4: Resolution Look in all leads for: Q waves Inverted T waves ST segment elevation or depression • Normal T wave upright when QRS upright • If T wave inverted, then = ischemia • Try and compare with old EKG to determine if inversion is new or old • ST elevation + Q waves = acute infarction • “Non-Q” MI = infarct without Q waves • ST often returns to baseline in time 6 hours from lumen blocked by clot to start of tissue death appears as ST elevation 6 hour period is when must start TPA (“clot busters”) to salvage heart tissue “Time is Muscle!” Qs represent progression of injury to infarction Pathologic Qs = QRS (-) deflection after PR interval & >1/3 size of QRS If ST elevations & Qs at same time, STEMI evolving from injury to necrosis Development of scar tissue in infarcted area occurs roughly 2 weeks after necrosis Affected part of heart may show EKG changes forever Be careful – flipped T waves can also mean pt having new ischemia! Persistent ST depression may indicate “Non-Q” MI Pacemakers Atrial or ventricular or both Looks like “spikes” on the ECG Be wary of the patient with a pacer who has no spikes Some EKG lead groups are electrical “mirrors” ST elevations in one group appear as depressions in the other group in two specific areas: Inferior and Lateral Septal & Posterior Elevations always come first If there are ST elevations on EKG, ST depressions on the same EKG might be reciprocal instead of ischemic V1 There are no true posterior leads on a standard EKG Septal leads look at anterior & posterior heart & “mirror” an infero-posterior infarction Remember the RCA perfuses inferior & posterior areas: V2 ST elevations in II, III, aVF? ST depressed in V1, V2? II III Most prominent feature are peaked-T waves “Sine waves” also seen Changes seen across ALL leads, not in a single coronary artery pattern Common with all electrolyte / metabolic abnormalities Anatomy plus electricity equals rhythm SA node origin Rate 60 – 100 beats/ minute > 100 = sinus tachycardia < 60 = sinus bradycardia If irregular, rate determined by both a “ventricular” & “atrial” rate Normal variant Irregular rhythm varies with respiration All P waves look identical Intrinsic rate for SA node: 60 - 100bpm Causes: Inferior MI (RCA lesion) Sedation Rhythm originates in the SA node P wave for every QRS Rate > 100 / minute Increased cardiac stress from systemic process: Hypovolemia / Hypotension Hypoxia Anxiety Drugs (i.e. cocaine) Exercise Rate 60 – 90 bpm Occasional “escape” ectopic beats Also known as “PACs” Atrial reentry from a circular conductive pathway Single ectopic pacemaker May have inverted P-waves Two or more asynchronous cardiac pacemakers The hallmark of this form of SVT is multiple Pwave morphologies (one from each pacemaker) Absence of p-waves before each QRS Irregularly irregular from ectopic foci with re-entry Rate ~ 200-300bpm No True P Waves Multiple sawtooth edged P waves before each QRS Many ectopic pacemakers Unstable rhythm May progress to atrial fibrillation • No P waves or atrial activity • Normal QRS • Ventricles generating slow escape rate (20-40 BPM) “Accelerated” IVR faster than expected rate (>60) Ventricular pacemakers speed up & capture as pacers are faster than the underlying rhythm SVT: Generated above ventricle P waves present Narrow VT: Generated in ventricles No P waves Wide Generated above ventricles so narrow complex with P waves May be normal in bursts in young, healthy individuals Often difficult to differentiate from VT •Wide QRS (>140 ms) without atrial activity / P waves •ANY wide tachycardia is VT until proven otherwise •Often caused by ischemic / infarcted conductive ventricular tissue causing a reentry tachycardia SVT Rhythm - Regular Rate - 140-220 BPM QRS Duration - normal P Wave - Buried in preceding T wave P-R Interval - Depends on site of supraventricular pacemaker Impulses stimulating heart are not generated by sinus node, instead from a collection of tissue around the AV node VT Rhythm - Regular Rate - 180-190 BPM QRS Duration - Prolonged P Wave - Not seen Abnormal ventricular tissues generating a rapid & irregular heart rhythm & poor cardiac output is Wide and slow No P waves as rhythm starts below atria <6 in a minute = Normal >6 in a row= Ventricular Tachycardia Multiple ventricular areas contract without coordination Quivering results in loss of cardiac output & death Cure for VF is electrical defibrillation Alan Lindsey ECG Learning Center in Cyberspace Dubin’s Guide to ECGs London Ambulance Sercice Unoffical ECG Guide Brady’s, Mosby’s, Caroline’s Prehospital Provider Textbooks www.TheMDSite.com Wikipedia, Google The ECG Guide (Iphone App) “Almost” everything you need to know: Part I: Cardiac Anatomy Review Part II: The Cardiac Cycle Part III: From One Beat to Many Part IV: Basic Rhythm Analysis Is this everything you truly need to know? Look at every strip, ECG & rhythm you can…you need to know “normal” before you can know “abnormal”