Ability is what you are capable of doing. Motivation determines what you do. Attitude determines how well you do it. - Lou Holtz

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1 Presented By: Cynthia Webner DNP, RN, CCNS, CCRN-CMC, CHFN Karen Marzlin DNP, RN, CCNS, CCRN-CMC, CHFN Ability is what you are capable of doing. Motivation determines what you do. Attitude determines how well you do it. - Lou Holtz 1

2 Let s continue on our journey!! 1 st CCU in the world opened in March 1962 was in Toronto, Canada In May of 1962 the 1 st CCU in the US opened at Bethany Hospital in Kansas City, Kansas by Dr. Hugh Day Early cardiac monitoring focused on observing heart rates and monitoring for life threatening arrhythmias Monitoring equipment has changed greatly over the past 50+ years 2

3 Dr. Desmond Julian opened 1 st CCU in Sydney Australia in Nov 1962 noted: All wards admitting patients with acute myocardial infarction should have a system capable of sounding an alarm at the onset of an important rhythm change and recording the rhythm automatically on an ECG.the provision of the appropriate apparatus would not be prohibitively expensive if these patients were admitted to special intensive care units. Such units should be staffed by suitably experienced people throughout the 24 hours. 3

4 Class I Recommendations Cardiac monitoring indicated in most, if not all, patients in this group. Class II Recommendations Cardiac monitoring may be of benefit in some patients but is not considered essential for all patients. Class III Recommendations Cardiac monitoring is not indicated because a patient s risk of a serious event is so low that monitoring has no therapeutic benefit. Despite advances in technology, the need for human over site in the interpretation of the ECG is as important as it was 50 years ago for the following reasons: With the high sensitivity capabilities of the current monitors numerous alarms must be evaluated to prevent over treatment More aggressive approaches to treatment of myocardial ischemia improves outcomes requiring ongoing surveillance Complex device technology requires expert analysis of ECG monitoring data Many more drugs have been that prolong QT intervals failure to identify patients at risk increases the incidence of sudden cardiac death Only humans not monitors can determine the goals of monitoring for individual patients 4

5 Dedicated monitor watcher Pros and cons Investing in advanced monitoring technology may be more cost effective than dedicated watchers Combination of monitors from several units at a remote site by a dedicated watcher Not recommended UNLESS expertise of the remote monitor watcher is superior; and training cannot be provided to nurses on each monitored unit. Pagers that signal the nurse with monitor alarms that displays arrhythmia is helpful Monitoring needs are different for each unit requiring different training for each unit Staff proficiencies should be determined based on unit population and purpose of monitoring Formal orientation to include both didactic and hands on practice with return demonstration Accurate electrode placement is an essential part of the orientation process 5

6 Nurses role in bedside monitoring Educating nurses to utilize clinical judgment and critical thinking skills to make determinations regarding the best lead selection for each individual patient. Decisions should be based on the patient and his/her condition. Normal Rhythms Intraventricular conduction defects Bundle branch blocks Aberrant conduction Tachyarrhythmias Supraventricular AV reentrant AV nodal reentrant A fib / flutter Multifocal atrial tachycardia Atrial tachycardia Junctional ectopic tachycardia Ventricular Accelerated V arrhythmias Nonsustainded / sustainted polymorphic VT Prolonged QT interval associated VT VF Bradyarrhythmias Premature complexes Supraventricular Ventricular Pacemaker Electrocardiology Failure to capture, pace, or sense Failure to capture both ventricles in biventricular pacing ECG abnormalities in acute myocardial infarction ST segment elevation or depression T Wave inversion Muscle or other artifacts 6

7 Automaticity Excitation Conduction Sinus node physiology AV node physioloyg Wide and narrow QRS complexes Observation with arrhythmias Sustained vs nonsustained Monomorphic vs polymorohic Stable vs nonstable Symptomatic vs asymptomatic Association with heart disease vs no heart disease Syncope Hemodynamic effects of arrhythmias Influence of rate Influence of heart disease Influence of A-V synchrony Influence of LV synchrony Function of Implantable devices Acute myocardial ischemia STEMI ST recovery of successful reperfusion Reperfusion arrhythmias NonSTEMI Transient ischemia Effects of common antiarrhythmic drugs, rate control vs rhythm control Operation of monitoring system Recognition of limitations of computerized algorhithms Proper skin prep Accurate lead placement Setting Gain Setting heart rate, ST alarm parameters Measurement of HR Measurement of intervals (with calipers) Recognition of atrial activity Evaluating pauses Diagnosis of specific rhythms Recording from postoperative epicardial wires Ability to intervene (unit protocols for responding, reporting, and documenting) in patients with: Bradycardia Tachycardia Syncope Cardiorespiratory arrest Implantable devices Temporary pacemakers Transcutaneous pacemakers Documenting arrhythmias Lead identification Onset and offset of arrhythmias Physician notification 7

8 The ECG is a graphic recording of electrical activity spreading through the heart 12 lead ECG provides 12 different views of electrical activity Each bedside monitoring lead provides one view 8

9 SA Node AV Node Bundle of His AV Junction Right and Left Bundle Branches Anterior and Posterior Fascicles Purkinge Fibers WAVES and COMPLEXES QRS P P wave: atrial depolarization QRS: ventricular depolarization T wave: ventricular repolarization PR interval: AV conduction time QRS width: intraventricular conduction time ST Segment: entire ventricular depolarization QT interval: used to reflect ventricular repolarization time QT Interval T PR Interval QRS ST Segment 9

10 Normal speed 25 mm/ sec Smallest box 1mm x 1mm 1 small box 0.04 sec 1 large box 0.20 sec 5 large boxes 1.0 sec Regular rhythms Count number of large boxes between R waves and divide into 300: 1 = = 50 2 = = 43 3 = = 37 4 = 75 9 = 33 5 = = =

11 4 big + 2 tiny = rate big boxes + 2 tiny boxes 22 11

12 Irregular rhythms Count number of R-R intervals in a 6 second strip and multiply by X 10 = Lead 1 avr V1 V4 + Left Arm High Lateral Wall LAD (Diagonal) Axis Quadrant + Right Arm P Wave always + 4 th ICS, RSB Septal Wall & RV LAD (Septal) Ectopy VS Aberrancy RBBB LBBB LVT RVT Reciprocal to Posterior + L MCL, 5 th ICS Anterior Wall LAD Lead 2 avl V2 V5 + Left Leg Inferior Wall RCA L Ant Hemi rs P Wave always + + Left Arm High Lateral Wall LAD (Diagonal) Reciprocal to Lead th ICS, LSB Septal Wall LAD (Septal) Reciprocal to Posterior + L anterior axillary, same level as V 4 Low Lateral Wall Circumflex (Marginal) Lead 3 avf V3 V6 + Left Leg Inferior Wall RCA L Ant Hemi rs Reciprocal to avl ST Segment Lead RCA + Left Leg Inferior Wall RCA L Ant Hemi rs Axis Quadrant + Midway Between V 2 & V 4 Anterior Wall LAD Reciprocal to Posterior ST Segment Lead LAD + L midaxillary line, same level as V 4 Low Lateral Wall Circumflex (Marginal) Ectopy VS Aberrancy RBBB LBBB ST Segment Lead Circ 12

13 Dual Electrode Leads Single Electrode Leads Dual Electrode Leads One positive electrode One negative electrode Records difference in electrical potential between selected electrodes Leads I, II, and III Single Electrode Leads One positive electrode One negative reference point Zero electrical potential Center of heart Leads avr, avl, avf V1-V6 13

14 Consider the positive pole of each lead as the camera (exploring electrode) RA RV LA - + LV + 14

15 Note: Nothing travels toward the right leg as a positive electrode. The right leg is the ground used to absorb any excess electrical activity. 15

16 Standard Limb Leads (Dual Electrode Leads) Leads I, II, III RA Left Arm + RA Left leg + _ Lead I + RA LA LA Left leg + + LL + 16

17 Augmented Limb Leads Leads avr, avl, avf Augmented Limb Leads (Single Electrode Leads) avr, avl, avf + RA LA + - Right Arm + LL + Left Arm + Left Leg + 17

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19 RA LV V6 RV + 4 th ICS, RSB + L MCL, 5 th ICS V5 + 4 th ICS, LSB + L anterior axillary, same level as V 4 V1 V2 V3 V4 + Midway Between V 2 & V 4 + L midaxillary line, same level as V 4 RA Left Arm + Right Arm th ICS, RSB + L MCL, 5 th ICS RA Left leg + Left Arm th ICS, LSB + L anterior axillary, same level as V 4 LA Left leg + Left Leg + + Midway Between V 2 & V 4 + L midaxillary line, same level as V 4 19

20 Posterior wall of the left ventricle and the right ventricle are not captured on the standard 12 lead ECG. 1. Septum depolarizes from left to right 2. Both ventricles depolarize from endocardium to epicardium 3. Basal portions of ventricles depolarize last 4. Mean direction of depolarization is downward, leftward, and posterior 20

21 If positive electrode sees depolarization approaching it, it records an upright complex If positive electrode sees depolarization heading away from it, it records a negative complex. Lead 1 avr V1 V4 + Left Arm High Lateral Wall + Right Arm + 4 th ICS, RSB Septal Wall + L MCL, 5 th ICS Anterior Wall Lead 2 avl V2 V5 + Left Leg Inferior Wall + Left Arm High Lateral Wall + 4 th ICS, LSB Septal Wall + L anterior axillary, same level as V 4 Low Lateral Wall Lead 3 avf V3 V6 + Left Leg Inferior Wall + Left Leg Inferior Wall + Midway Between V 2 & V 4 Anterior Wall + L midaxillary line, same level as V 4 Low Lateral Wall 21

22 THE SAME Importance of electrode placement The concept of the camera WHAT IS DIFFERENT Bedside monitor usually requires lead selection from among the 12 leads Must assure leads are identified on posted rhythm strips Many Options: 3 lead 5 lead 6 lead Derived ECG Hard Wired Telemetry 22

23 E: Lower extreme of the sternum (Brown +) A: Left mid-axillary line, same transverse line as E (Black +) S: Sternal manubrium (Red -) I: Right mid-axillary line, same transverse line as E (White -) G: Fifth electrode is the ground and can be placed anywhere on the torso (Green no polarity) Arrhythmia Detection Ischemia Monitoring QT Interval Monitoring 23

24 Candidates Primary purpose for all patients on cardiac monitor Purpose Detection of and prompt intervention for life threatening arrhythmias Best Leads V1 (or MCL1 if 3 lead cable) V6 (or MCL6) 24

25 Patients resuscitated from cardiac arrest Patients in early phase of Acute Coronary Syndromes (including Rule Outs ) Patients with unstable coronary syndromes and newly diagnosed high-risk coronary lesions Adults and children who have undergone cardiac surgery Patients after nonurgent percutaneous coronary interventions with complications Patients after ICD implant or pacer lead placement if pacer dependent Patients with temporary pacemaker or transcutaneous pacing pads Patients with AV block Patients with Arrhythmias complicating Wolff- Parkinson-White Syndrome with rapid anterograde conduction over an accessory pathway Patients with Long-QT Syndrome and associated ventricular arrhythmias Patients with intraaortic balloon pump Patients with acute heart failure/ pulmonary edema Patients with indications for intensive care Patient under going diagnostic / therapeutic procedures requiring conscious sedation or anesthesia Patients with any other hemodynamically unstable arrhythmias Diagnosis of arrhythmias in pediatric patients 25

26 Ectopy versus Aberrancy Lead 1 avr V1 V4 + Left Arm High Lateral Wall + Right Arm + 4 th ICS, RSB Septal Wall VT vs Aberrancy + L MCL, 5 th ICS Anterior Wall Lead 2 avl V2 V5 + Left Leg Inferior Wall + Left Arm High Lateral Wall + 4 th ICS, LSB Septal Wall + L anterior axillary, same level as V 4 Low Lateral Wall Lead 3 avf V3 V6 + Left Leg Inferior Wall + Left Leg Inferior Wall + Midway Between V 2 & V 4 Anterior Wall + L midaxillary line, same level as V 4 Low Lateral Wall VT vs Aberrancy 26

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28 Wide complex tachycardia presumed to be VT if diagnosis is unclear Don t assume VT cannot be well tolerated! The rate, size of the heart and presence of additional complications are often more important than the source of the tachycardia Check the patient (need to defib?) Check the blood pressure (need to cardiovert?) Check the ECG (determine the rhythm) Patient history / assessment QRS Width AV Dissociation Concordance Axis Morphology Note: VT is much more common than supraventricular tachycardia with bundle branch aberration. In wide QRS tachycardias VT is the right answer up to 80% of the time. 28

29 Acute ischemia / injury (Abnormal automaticity) Post myocardial infarction / ischemic cardiomyopathy (Reentrant circuit within myocardium) Non ischemic dilated cardiomyopathy (Bundle branch reentrant VT) The wider the QRS VT is favored However: SVT with LBBB will have a wider QRS than SVT with RBBB QRS will be wider in pre-existing BBB Other causes of SVT with wider than expected QRS: antidromic tachycardia and patients on Class IC or IA antiarrhythmics or amiodarone Not all VT is significantly wide VT originating from septum more narrow than VT from free wall If QRS more narrow than sinus rhythm = VT Independent atrial and ventricular activity (AV dissociation) is diagnostic for ventricular ectopy Ventricular tachycardia may also have retrograde P waves (retrograde P waves do not confirm VT) 29

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31 Axis Right Superior (Extreme / Northwest) axis deviation is strong indicator of ventricular ectopy Ventricular tachycardia rarely occurs with normal axis Ventricular tachycardia can occur with right or left axis deviation Use Lead I and avf Left hand represents QRS in Lead I Right hand represents QRS in avf Fingertips will point in the same direction as the QRS complex If hands are different, always place the left hand over the right. Handy Method of Axis Calculation developed by J. Cooper, PhD., American College of CV Nursing 31

32 I avf I avf I I avf avf Lead 1 avr V1 V4 + Left Arm High Lateral Wall + Right Arm + 4 th ICS, RSB Septal Wall VT vs Aberrancy + L MCL, 5 th ICS Anterior Wall AXIS Lead 2 avl V2 V5 + Left Leg Inferior Wall + Left Arm High Lateral Wall + 4 th ICS, LSB Septal Wall + L anterior axillary, same level as V 4 Low Lateral Wall Lead 3 avf V3 V6 + Left Leg Inferior Wall + Left Leg Inferior Wall AXIS + Midway Between V 2 & V 4 Anterior Wall + L midaxillary line, same level as V 4 Low Lateral Wall VT vs Aberrancy 32

33 Wide Complex Tachycardia: Ventricular Ectopy or SVT with BBB Aberration Morphology Challenges: BBB Reentrant VT Idiopathic RVOT Antidromic tachycardia LBBB RBBB LVT RVT V1 and V6 are gold standard monitoring leads for ectopy versus aberrancy Bundle branch block patterns and ventricle ectopy can be differentiated by using the morphology of these leads. DON T rely on Lead II!! 33

34 Standard 6 Lead Placement 34

35 MCL6 Standard 5 Lead Placement V1 & V6 Modified 5 lead Placement V1 & MCL6 Monitor Settings: V and III 35

36 Not every QRS complex contains a Q wave, R wave and S wave!! Q always negative (below baseline) R first positive above the baseline R second positive above the baseline S always negative deflection following the R wave or second component to entirely negative [[; /complex Let s Practice QS qr QR Qr qrs R RS rs Rs rsr 36

37 2 V 6 1 QRS sec V 1 37

38 V 6 = qrs V6 V 1 = rsr V1 QRS =.12 sec or more rsr qr 38

39 V 6 = wide R V 1 = QS V6 V1 QRS =.12 sec or more V1 = rs Nadir is the distance from the onset of the QRS complex to the lowest point of the S Wave Measure from the beginning of the QRS complex to the bottom valley or peak of the QRS The nadir in V1 should be < 0.06 sec for LBBB (slick down stroke) 39

40 RBBB LBBB Left ventricle first Right ventricle first VT from Left Ventricle VT from Right Ventricle Left ventricle first Right ventricle first Right Bundle Branch shaped R wave with an early left peak (Rr ) R wave with a single peak q wave followed by R wave 40

41 LBBB shaped Primarily negative wide rs complex delay to the nadir > 0.06 sec r wave broader than 0.03 sec Slurring on the down stroke Note: LBBB shaped VT can come from RV or septum. VT from RV includes: Idiopathic VT, BB Reentrant VT, Arrhythmogenic right ventricular dysplasia, VT from Brugada Syndrome VT with RBBB pattern or LVT VT with LBBB pattern or RVT 41

42 RBBB with Aberration LBBB with Aberration VT from Left Ventricle VT from Right Ventricle RBBB LBBB 42

43 Left Ventricular Tachycardia Right Ventricular Tachycardia QS complex r wave followed by S wave with R:S ratio < 1 - Any Q Wave - QS wave SVT RBBB SVT LBBB VT VT 43

44 SVT RBBB SVT LBBB LVT RVT 44

45 SVT RBBB SVT LBBB LVT RVT SVT RBBB SVT LBBB LVT RVT 45

46 SVT RBBB SVT LBBB LVT RVT SVT RBBB SVT LBBB LVT RVT 46

47 SVT RBBB SVT LBBB LVT RVT SVT RBBB SVT LBBB LVT RVT 47

48 SVT RBBB SVT LBBB LVT RVT SVT RBBB SVT LBBB LVT RVT 48

49 SVT RBBB SVT LBBB 12 Lead ECG Post Inferior STEMI on Arrival to CCU LVT RVT Read as Atrial Fibrillation with RBBB and LAHB. 49

50 SVT RBBB SVT LBBB LVT RVT SVT RBBB SVT LBBB 12 Lead ECG Post Inferior STEMI on Arrival to CCU Vital Signs Stable 12 lead ECG Interpretation: Non Specific Intraventricular Conduction Delay?? LVT RVT 50

51 STRIP 1 STRIP 2 STRIP 1 STRIP 2 51

52 V1 III ABOVE: VT with incorrect lead placement. BELOW: VT with correct lead placement. V1 SVT RBBB SVT LBBB LVT RVT 52

53 I avr V1 V4 II avl V2 V5 III avf V3 V6 53

54 . Importance of Alarm Review! These arrhythmias were discovered while preparing a patient for discharge. EP consulted. Antiarrhythmics (excluding beta blockers) not used as primary therapy for prevention of SCD Patients with VT who do not meet criteria for ICD Patients with ICD with recurrent VT Beta Blockers Suppresses ventricular arrhythmias Mortality benefit Amiodarone Suppresses ventricular arrhythmias No definite survival benefit Complex drug interactions and many adverse side effects Sotalol Suppresses ventricular arrhythmias No definite survival benefit More pro-arrhythmic than amiodarone 54

55 Stable Ventricular Tachycardia (Preserved LV Function) Monomorphic Procainamide Sotalol * Amiodarone Lidocaine Polymorphic Normal QT Beta Blockers (or) Lidocaine (or) Amiodarone (or) Procainide (or) Sotalol (or) Polymorphic Prolonged QT Magnesium (or) Lidocaine (or) Isoproterenol (or) Phenytoin (or) Stable Ventricular Tachycardia impaired cardiac function * Amiodarone (or) Lidocaine V-fib seldom is seldom preceded by warning arrhythmias Prophylactic lidocaine not indicated R on T PVCs are typically only important first 24 hours of myocardial infarction Bigeminy may need treated if cardiac output effected Ventricular ectopy (as infrequent as 15% burden) can result in heart failure 55

56 Potential reversible causes Hypokalemia: K < 3.2 meq/l (cause or result) Magnesium < 1.5 meq/dl Ischemia Use of inotropic agents Three Reasons for Bedside Cardiac Monitoring Arrhythmia Detection Ischemia Monitoring QT Interval Monitoring 56

57 Left Main Coronary Artery (LM) Left Anterior Descending Artery (LAD) Diagonal Branch Septal Perforator Left Circumflex Artery (LCirc) Obtuse Marginal (OM) Ramus intermedius Right Coronary Artery Marginal Branch Posterior Descending Artery (PDA) Concept of dominance LAD Anterior LV High Lateral LV Septum (anterior 2/3) Bundle Branches Left Circumflex Low Lateral LV Posterior LV Left Atrium Anterolateral papillary muscle of the mitral valve SA Node (45%) AV Node (10%) 57

58 RCA Inferior LV Septum (lower 1/3) Right Ventricle (marginal branch) Posterior LV (PDA) Posterior LBB Posteromedial papillary muscle Right Atrium SA Node (55%) AV Node (90%) Purpose To monitor changes in ST segments (compared to baseline) in select leads Leads of Choice Based on area of known or potential ischemia Anterior wall / Left anterior descending coronary Lead V3 Inferior wall / Right Coronary artery Lead III Lateral wall / Circumflex coronary artery Lead V6 Supply and demand ischemia Lead V5 58

59 Lead 1 avr V1 V4 + Left Arm High Lateral Wall + Right Arm + 4 th ICS, RSB Septal Wall VT vs Aberrancy + L MCL, 5 th ICS Anterior Wall Lead 2 avl V2 V5 + Left Leg Inferior Wall + Left Arm High Lateral Wall + 4 th ICS, LSB Septal Wall + L anterior axillary, same level as V 4 Low Lateral Wall Lead 3 avf V3 V6 + Left Leg Inferior Wall ST - RCA + Left Leg Inferior Wall + Midway Between V 2 & V 4 Anterior Wall ST - LAD + L midaxillary line, same level as V 4 Low Lateral Wall VT vs Aberrancy ST - Circ Patients in early phase of Acute Coronary Syndromes (including Rule Out ) Patients who present to ED with chest pain or anginal equivalent symptoms Patients who have had nonurgent percutaneous coronary interventions with suboptimal results Patients with possible variant angina resulting from coronary vasospasm 59

60 Patients postacute MI Patients after nonurgent uncomplicated percutaneous coronary intervention Patients at high risk for ischemia after cardiac or noncardiac surgery Pediatric patients at risk of ischemia or infarction resulting from congenital or acquired conditions Patients with left bundle branch block Patients with ventricular paced rhythms Patients with other confounding arrhythmias that obscure the ST Segment Patients who are agitated 60

61 Revised 2009 Identification of body position changes Careful skin preparation Consistent lead placement Tailoring alarm parameters to patients baseline ST level Understand goals of monitoring in the individual patient Analyze ECG print out rather than just graphic trends 61

62 STs may fluctuate with body position changes May cause false alarms ST should be evaluated with patient in the supine position ECG noise impedes accurate diagnosis Skin prep essential to good tracing Clipping to remove hair Remove skin oils with abrasion (dry 4x4) Keep electrodes in original package start to dry 20 minutes after opening Mark electrode placement Waveform changes may occur with as little as 1cm change in location Assess change in ST for true change or change lead location Alarms must be set to reflect each individual patient s baseline 1mm above and below for precordial leads 0.5 mm for limb leads 2mm reasonable in the more stable patient (helps eliminate false alarms) Monitor for silent ischemia Monitor for recurrent ischemia Bad Alarm Monitor for ST recovery after intervention with fibrinolytic or PCI Good Alarm Graphic trends are capable on most monitors with ST segment monitoring Convenient for quick identification of ischemia Should never replace evaluation of rhythm strips When in doubt always verify with a 12 lead ECG 62

63 Voltage or amplitude Measured in millivolts(mv) or millimeters (mm) EKG machine calibrated so that 1 mv produces a deflection measuring exactly 10 mm tall 1 small box = 1 mm high 1 large box = 5 mm high In limb leads the ST segment is normally isoelectric but may be slightly elevated or depressed by less than 1mm In precordial leads ST segment elevation is normally not more than 1 to 2 mm (small elevation normal in many people) 63

64 Point where the QRS complex and the ST segment meet. ST segments are measured 60 to 80 msec from J point to avoid atrial repolarization wave. 64

65 Represents ventricular repolarization Slightly asymmetrical Usually upright Most likely abnormal If inverted in two contiguous leads Not normally > than 5mm (limb leads) to 10 mm (precordial) high 1) Assess for ST segment elevation first ST elevation and need for reperfusion 2) Assess for T wave inversion next Non STEMI or Unstable angina ischemia 3) Assess for ST segment depression thirdly Supply and demand ischemia (often in V5 regardless of vessel occlusion) OR reciprocal changes to ST elevation Clinical application: Supply and demand ischemia is typically not the primary problem in patients at rest 65

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68 T wave should be positive in lead I and II Inversion in lead III, avl and avf may be normal Inversion in V1 is common - always compare to previous ECG 68

69 Wellen s Warning when seen in chest leads(v2-v3) of undiagnosed patient Represents LAD occlusion that spontaneously reperfused prior to the ECG (lesion at risk for reocclusion) Seen on ECG done during pain free period Can be UA / NSTEMI 69

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71 Can be seen in exercise stress testing with supply and demand ischemia. Often seen with left ventricular hypertrophy. 71

72 ECG Be suspicious of horizontal ST segment depression in patient at rest. Suspect left main disease (or significant 3 vessel disease) when diffuse depression and ST elevation in lead avr (and V1 to lesser extent) Presentation Assess for reasons for supply and demand ischemia at rest (i.e. low hemoglobin). Rule out medical reason for falls, motor vehicle crashes, and other trauma (i.e. syncope or near syncope due to cardiac cause). T wave inversion is a warning for ACS (either unstable angina or NonSTEMI) unless T wave inversion occurs after a STEMI After a STEMI T wave inversion is expected Terminal T wave inversion is a sign of reperfusion after a STEMI Symmetrical T wave inversion will develop after terminal T inversion 72

73 Evolutionary changes occur due to prolongation of the cardiac action potential in regions of stunned myocardium adjacent to the necrotic area. Prolongation in repolarization affects the voltage and polarity of the T wave. Ventricular remodeling can produce differences in electrical fields that may be responsible for the evolutionary changes. 73

74 ST segment back to baseline occurs as result of myocardial cell death and reduction in injury current. One of final evolutionary changes. Abrupt resolution of ST elevation indicates reperfusion. Persistent ST elevation is predicator of adverse outcomes. 74

75 ST segment back to baseline occurs as result of myocardial cell death and reduction in injury current. One of final evolutionary changes. Abrupt resolution of ST elevation indicates reperfusion. Persistent ST elevation is predicator of adverse outcomes. 75

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77 18 Hours Post STEMI Lead III 36 Hours Post STEMI Lead III 77

78 A SUCCESS Story!! The next 2 slides show the following: 1. Admission ECG for a patient with an anteroseptal / lateral wall STEMI. 2. ECG post intervention for same patient. 1. Note: The T waves have not yet inverted post intervention. Ideally T waves will begin to invert after an intervention showing evidence of reperfusion. REMEMBER: T wave must invert within hours after a STEMI (the sooner the better). Failure of T waves to invert after a STEMI is indicative of post infarction regional pericarditis and the patient is at higher risk for myocardial rupture. 78

79 The strip below assessing ST segments in V3 was done 48 hours post STEMI (same patient as previous 2 ECGs.). The failure of the T waves to invert is indicative of post infarction regional pericarditis with increased risk of myocardial rupture. The patient was hypotensive, which raises the concern for cardiac tamponade as the etiology of the hypotension. This assessment finding was communicated to the cardiologist. The patient s echocardiogram showed a large pericardial effusion and the patient subsequently underwent a surgical pericardial window. 79

80 Primary Change is most important look for: ST Elevation: ACS (STEMI) T Wave Inversion: ACS (Non STEMI or UA) ST Depression (ischemia) Reciprocal Changes ST segment depression in leads reciprocal (opposite) those with ST elevation Reciprocal changes can help confirm primary changes 80

81 Lead 1 avr V1 V4 Left Arm High Lateral Wall Right Arm 4 th ICS, RSB Septal Wall L MCL, 5 th ICS Anterior Wall Posterior Wall Lead 2 avl V2 V5 Left Leg Inferior Wall Left Arm High Lateral Wall 4 th ICS, LSB Septal Wall L anterior axillary, same level as V 4 Low Lateral Wall Lead 3 avf V3 V6 Left Leg Inferior Wall Left Leg Inferior Wall Midway Between V 2 & V 4 Anterior Wall L midaxillary line, same level as V 4 Low Lateral Wall 81

82 These are vulnerable areas of myocardium: Not directly assessed on 12 Lead! 82

83 V3 V8 VI V4 V2 V5 V3 V6 83

84 VIR V4R V2R V5R V3R V6R Right Ventricular Leads Posterior Leads 84

85 Place electrode in V4R Position 5 th ICS Right MCL Attach V monitoring lead (Brown Lead) to electrode Assure monitor lead selector is on V Run strip and clearly mark V4 Right Chest Lead Place electrode in V8 position Under tip of left scapula same level as V6 Attach V monitoring lead (Brown Lead) to electrode Assure monitor lead selector is on V Run strip and clearly mark V8 Posterior Lead Patient post cardiac arrest on hypothermia. 85

86 Same Patient as Previous 12 Lead: Due to hypotension the point of care nurse used the V lead from bedside monitoring to record a V4R lead. This recording confirms RV injury and this knowledge was used to guide treatment. ST segment elevation in lead V4R demonstrates high risk for high grade AV node block (Wellen & Conover, 2006). 86

87 Support for Continuous ST Segment Monitoring 61 year old Caucasian male with increasing SOB and cough for 2-3 days. Treated by his PCP with ATB, Tessalon Perles and Flonase for asthmatic bronchitis. Presented to ED (via EMS) later that evening with severe DOE. Was hypoxic on arrival. + cough with yellow sputum, wheezing, SOB. Admitted and placed on IV steroids of bronchitis. 87

88 Obstructive sleep apnea (noncompliant with CPAP) HTN Psoriatic arthritis DM, Type II Obesity Tobaccoism ETOH use (daily) Troponin 0.01, 0.02, 0.14 Myoglobin 89, 323 WBC 15,000; Hgb 13.9; Plt 239,000 Glucose 419, Na 135, BUN 17, Cr 1.16, K 4.4 Rapid flu neg CXR: no acute process 88

89 Symptoms did not suggest ACS, but due to risk factors another troponin was drawn. Troponin bump was felt to be due to hypoxia. A Lexiscan stress test was recommended once his pulmonary status improved. 89

90 Troponin 0.36 Patient more SOB Repeat ECG ordered Patient down in heart lab for echocardiogram. ECG done 1 hour later. 90

91 Patient emergently to the cardiac cathetrization lab (called as a STEMI) and received PCI with DES to RCA (100% occluded). EF 55%. Was also a RV infarct 91

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102 Three Reasons for Bedside Cardiac Monitoring Arrhythmia Detection Ischemia Monitoring QT Interval Monitoring Action Potential of Cardiac Cells Phase 0: Rapid depolarization Sodium Influx (beginning of QRS complex) Phase 1: Brief, rapid initiation of repolarization 102

103 Phase 2: Slowing of the repolarization Calcium Influx correlates with ST segment Phase 3: Sudden acceleration in the rate of repolarization - Potassium Efflux Correlates with T wave Phase 4: Resting membrane potential 103

104 1 to 15 Years Adult Males Adult Females Normal <.44 seconds <.43 seconds <.45 seconds Borderline.44 to.46 seconds.43 to.45 seconds.45 to.47 seconds Prolonged >.46 seconds >.45 seconds >.47 seconds Source: Moss AJ, Robinson JL. Long QT Syndromes. Heart Dis Stroke. 1992; QTc.50 sec (500 msec or more is dangerous and should be considered an ominous sign of impending Torsade's de Pointes) 104

105 Purpose To monitor for increase in QT interval to identify and intervene in patients at high risk for Torsades de Pointes Leads of Choice Lead where an accurate QT Interval can be measured V2 and V3 usually have the longest QT T wave is often clearest V5 or V6 For repetitive QT interval monitoring in an inpatient setting: Pick a lead with a well defined T wave Use the same lead consistently Patient can be changed to another lead to run a strip to measure QT or 12 lead can be done if QT not easily measured in V1 or V 6 QT prolongation > 500 msec common in hospitalized patients (ICU and progressive care) (24%) QT prolongation associated with longer length of stay QT prolongation associated with almost 3 times the odds for mortality (Pickham et al., 2012, Critical Care Medicine) 105

106 Patients administered an antiarrhythmic drug know to cause Torsades de Pointes Patients who overdose from a potentially proarrhythmic agent Patients with new onset bradyarrhythmias Patients with severe hypokalemia or hypomagnesemia Patients who require treatment with antipsychotics or other drugs with possible risk of Torsades de Pointes Patients with acute neurologic events Healthy patients administered drugs that pose little risk for Torsades de Pointes 106

107 Measured from beginning of QRS complex to the end of the T wave Reflects both ventricular depolarization (QRS) and ventricular repolarization (T wave) Used most specifically to reflect ventricular repolarization Role of QRS width in QT interval Manual versus computer generated measurement Continuous QT interval monitoring software U waves End of T wave in biphasic T wave Which lead for measurement RR interval in irregular rhythms Calculated measurement via 12 Lead ECG Bedside monitor calculation via e-calipers 107

108 U Waves and Biphasic T waves. QT interval needs to be adjusted for HR QT does not adjust to HR on a beat to beat basis Dynamic changes are most important Abnormal findings are uncovered during abrupt changes in the R to R Irregular heart rhythms (i.e. atrial fibrillation) remain a clinical challenge 108

109 Print a long rhythm strip to assess over the course of the strip if the interval from the R wave to the peak of the following T wave is more than 50% of the proceeding RR interval. If so this is considered too long a QT interval and the risk for Torsades de Pointes is increased. Source: Sommargren & Drew, Bazett Formula Formula not reliable at slow rates (under estimates); over estimates QT interval at fast HRs Measurements are using seconds. Other Formulas proposed to be superior Fridericia Framingham Nomogram 109

110 Places of unequal repolarization can set up for reentrant tachyarrhythmias There can be the development of early after depolarizations Right after repolarization (or during) there is a transient sub threshold depolarization Can occur during Phase II or III of the cardiac action potential If an early after depolarization reaches threshold a second upstroke occurs and a triggered beat follows The triggered beat may have its own after depolarization that reaches threshold thus causing another triggered beat Thought to be etiology of Torsade's de Pointes Acquired Congenital 110

111 Precipitating Factors Hypokalemia Hypomagnesemia Heightened sympathetic tone Slow heart rate Prolonged repolarization (QT interval) 111

112 Long QT Syndrome (LQTS) Brugada disease Idiopathic short QT < 300 to 340 msec Diagnosed by family history and ECG Note: Patients with heart failure can develop channelopathies 224 QTc > 450 ms Genetic defect in either potassium (LQT1 or LQT2) or sodium (LQT3) channels Delayed repolarization (1 and 2) LQT1 and LQT2 = 95% Beta blockers LQT3 = 5% Beta blockers may be harmful Autosomal dominant trait 1 in 2500 QT prolongation important risk factor for SCD QTc < 440 ms / < 5% QTc 460 to 500 ms / 20% QTc > 500 ms / 50%

113 Interestingly some acquired Torsade's may be preceded by T wave morphology looking like congenital LQTS Long QT 1: wide, broad-based T waves Long QT 2: low amplitude, often notched T waves Long QT 3: long ST segment and tall, peaked T waves 113

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115 Disorder of cardiac sodium channel Autosomal dominant Most common in Asia Typical patient young male age 30 to 50 who is otherwise healthy. ST elevation in anterior precordial leads Cove Saddleback ECG can be dynamic In children temperature spike may uncover Treat aggressively Syncope 2 year risk of SCD approximately 30% ICD recommended

116 232 Recognition of this life-threatening arrhythmia is important because it is not treated like other VTs Two groups: Acquired and congenital Acquired Drugs prolonging repolarization Most often as a result of blocking the potassium channel Electrolyte abnormalities Low potassium Low magnesium Severe bradycardias / pauses 116

117 Class Ia and Class III antiarrhythmics Antihistamines Antibiotics Antipsychotics Antidepressants Sedatives Gastric motility agents Anticancer agents Opiate agonists Risk Possible Risk Conditional 117

118 Rapid (IV) administration of QT prolonging agent Renal or hepatic dysfunction Female gender (particularly for drug induced) Advanced age Anorexia Heart disease Poly pharmacy Simultaneous 2-lead ECG (leads II and V1) showing initiation and termination of torsade de pointes in patient in AF after ibutilide infusion. VanderLugt J T et al. Circulation. 1999;100: Copyright American Heart Association, Inc. All rights reserved. 118

119 Increase QTc from predrug baseline of 60 ms, Marked QTc interval prolongation.500 ms T-U wave distortion that becomes more exaggerated in the beat after a pause Visible (macroscopic) T-wave alternans New-onset ventricular ectopy, couplets Nonsustained polymorphic ventricular tachycardia initiated in the beat after a pause. 119

120 Class I Discontinue offending drugs Magnesium is considered treatment of choice. Note: Class IA drug induced TdP usually appears soon after the initial administration of the drug Correct electrolytes Magnesium Potassium Increase HR Isoproteronol Temporary pacing at rate of 100 to 110 Pacing if bradycardia or CHB cannot be resolved. Defibrillation if sustained 120

121 2 Gm IV bolus over 1-2 minutes Followed in 15 minutes by another bolus if necessary May start continuous infusion at rate of 3-20 mg/min Benefit occurs without shortening of QT interval and in presence of normal Magnesium level 121

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123 Patient admitted for syncope after having motor vehicle crash while driving. Long standing history of paroxysmal atrial fibrillation on dofetilide (Tykosin) for several years. Recent chemotherapy for breast CA resulting in a reduction of EF. Recent increase in carvedilol and lisinopril per general cardiology to improve EF. Next slide is admission ECG. Note the QTc interval.. 123

124 1. Strip 1: QTc consistent with admission ECG. 2. Strip 2: Marked QTc prolongation when patient asleep. 3. Initial run of ventricular tachycardia initiated by PVC firing at end of T wave, Same patient with sustained Torsades de Pointes. Treated effectively with 2 grams IV Magnesium (magnesium level was normal at baseline). Magnesium is the drug of choice to stabilize the cardiac membrane. Dofetilide (Tikosyn) was also discontinued. Note: Although the patient had been on dofetilide (Tikosyn) for several years, the recent change in ejection fraction and increase in beta blocker therapy increased her risk for Torsades de Pointes. 124

125 Seen frequently in ischemic conditions Think revascularization Think beta blockers DC cardioversion with sedation when unstable IV beta-blockers if ischemia suspected Improve mortality IV amiodarone in absence of abnormal repolarization Amiodarone better than placebo Magnesium not better than placebo Urgent angiography to exclude ischemia Lidocaine may be reasonable if ischemia suspected Check electrolytes Consider any other potential reversible cause 125

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127 The Lewis Lead When P waves are not clearly seen in a rhythm strip (see lead 3 above), the Lewis lead can be very helpful in assessing for the presence of atrial activity. As seen in the Lewis lead above this patient is clearly in an atrial flutter. The atrial flutter is not as obvious in the lead III rhythm strip. V1 MCL6 MCL6 127

128 Telemetry Pack R A Lead 1 L A 128

129 60 to 70% of WPW shows evidence in SR Left sided accessory pathway: Positive delta wave in V1 Right sided accessory pathway: Negative delta wave in V1 Arrhythmias of WPW (AVRT or CMT) 129

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131 Slows conduction through the AV Node Vasodilator Interrupts reentry pathways through the AV node and restores sinus rhythm Uses: Paroxsysmal SVT, AVNRT, Drug stress testing Side Effects: Headache, arrhythmias (blocks), SOB, chest pressure Nursing Considerations: Use cautiously in patients with asthma could cause bronchospasm Onset IV: Immediate Peak: 10 sec Duration seconds Dosing for conversion of arrhythmia: 6mg IV rapid push If no change within 1-2 minutes repeat with 12mg rapid push Not indicated in WPW 131

132 Atropine will not work when the block is below the level of the AV node (meaning the block is in the His Perkinje system) Second degree type two block High grade AV block below the level of the AV node escape Complete heart block with ventricular escape rhythm Both of these examples: 1. One P wave at a time fails to conduct 2. There is a fixed PR interval 3. There is a wider than normal QRS 132

133 Critical Thinking Guideline for Cardiac Monitoring 133

134 Patient Characteristics Ejection fraction < 30% Implantable cardioverter defibrillator Non ischemic cardiomyopathy Syncope as reason for admission Current frequent premature beats or short runs of tachycardias Monitoring Priorities Arrhythmia monitoring: Use V1 and V6 (or MCL6) as primary monitoring leads. Patient Characteristics Stable acute coronary syndrome (ACS) or rule out ACS as reason for admission Admission symptoms suspicious for ischemia (shortness of breath, nausea, fatigue, etc) Admission with heart failure with history of recent revascularization Monitoring Priorities Ischemic monitoring: Use V3 and lead III as primary ischemia detection leads if area of ischemia or culprit vessel is unknown. If known, choose ischemia monitoring leads based on ECG footprint during active ischemia document reason for use of chosen leads. Perform ECG with posterior leads (or record lead V 8 ) during symptomatic episodes with non diagnostic standard 12 Lead. Simultaneously monitor in V1 for arrhythmia detection for patients admitted to ICU or step down level of care. Note: Whenever possible in ICU and step down level patients a 6 lead telemetry system should be used in order to monitor V1 for arrhythmia detection and the second V lead for ischemia monitoring. 134

135 Patient Characteristics New administration of class I or class III antiarrhythmics Electrolyte abnormalities (hypokalemia, hypomagnesemia, hypocalcemia) QTc >.45 seconds Receiving Haldol or other high risk medications Monitoring Priorities Use arrhythmia monitoring leads as baseline monitoring leads (V1 & V6). Measure QTc interval q 4 hours with rhythm interpretation in lead where QT interval can be clearly defined. Document and record lead used for measurement. Use consistent lead in the measuring of QTc. Patient Characteristics High risk (hemodynamic or electrical instability) ACS Monitoring Priorities V1 for arrhythmia assessment Secondary monitoring can be a limb lead or modified chest lead to aid in either arrhythmia interpretation or ischemia detection. 135

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141 BE THE BEST THAT YOU CAN BE EVERY DAY. YOUR PATIENTS ARE COUNTING ON IT! 141