Presentation on theme: "Rhythm & 12 Lead EKG Review"— Presentation transcript:
1 Rhythm & 12 Lead EKG Review March 2011 CECondell Medical CenterEMS SystemSite code # E-1211Prepared by: FF/PMD Michael Mounts – Lake Forest FireRevised By: Sharon Hopkins, RN, BSN, EMT-P
2 ObjectivesUpon successful completion of this module, the EMS provider will be able to:Identify the components of a rhythm stripIdentify what the components represent on the rhythm stripIdentify criteria for sinus rhythmsIdentify criteria for atrial rhythmsIdentify AV/junctional rhythms
3 Objectives cont. Identify ventricular rhythms Identify rhythms with AV blocksIdentify treatments for different rhythmsIdentify criteria for identification of ST elevation on 12 lead EKG’sIdentify EMS treatment for patients with acute coronary syndrome (ST elevation)Demonstrate standard & alternate placement of ECG electrodes for monitoring
4 Objectives cont.Demonstrate placement of electrodes for obtaining a 12 lead EKGDemonstrate the ability to identify a variety of static or dynamic EKG rhythm stripsDemonstrate the ability to identify the presence or absence of ST elevation when presented with a 12 lead EKGReview department’s process to transmit 12 lead EKG to hospital, if capableSuccessfully complete the post quiz with a score of 80% or better.
5 ECG Paper What do the boxes represent? How do you measure time & amplitude?Time is measured horizontally. Amplitude, or voltage, is evaluated by number of boxes cumulatively above/below the baseline. Amplitude, or voltage, is the strength of the current.
6 Components of the Rhythm Strip ECG PaperWave formsWave complexesWave segmentsWave intervals
7 Wave Forms, Complexes, Segments & Intervals P wave – atrial depolarizationQRS – Ventricular depolarizationT wave – Ventricular repolarizationDepolarization does not guarantee that a contraction occurred. Contractions must be evaluated by feeling for a pulse and measuring the blood pressure. Depolarization is an electrical response and contractions are a mechanical response.
8 What’s a J point and where is it? J point – point to mark end of QRS and beginning of ST segmentEvaluate ST elevation 0.4 seconds after J pointBased on relationship to the baseline
9 Intervals and Complexes PR interval – atrial and nodal activityIncludes atrial depolarization & delay in the AV node (PR segment)QRS complexCorresponds to the patient’s palpated pulseLarge in size due to reflection of ventricular activity
10 The Electrical Conduction System AV NodeBundle of HISLeft Bundle BranchSA NodeRight Bundle BranchPurkinje FibersSA node is heart’s dominant pacemaker site with an inherent rate of beats per minute. As you move down the conduction system, the pacemaker site becomes slower and is less reliable.Inherent rates:SA nodeAV node 40-60Ventricles 20-40
12 Sinus Rhythms Originate in the SA node Inherent rate of 60 – 100 Normal sinus rhythm (NSR)Sinus bradycardia (SB)Sinus tachycardia (ST)Sinus arrhythmiaInherent rate of 60 – 100Base all other rhythms on deviations from sinus rhythm
21 Multifocal Atrial Tachycardia (MAT) (Rapid Wandering Pacemaker) Similar to wandering pacemaker (< 100)MAT rate is >100Usually due to pulmonary issueCOPDHypoxia, acidotic, intoxicated, etc.Often referred to as SVT by EMSRecognize it is a tachycardia and QRS is narrow
24 Wolff–Parkinson–White - WPW Caused by an abnormal accessory pathway (bridge) in the conductive tissueMainly non-symptomatic with normal heart ratesIf rate becomes tachycardic ( ) can be lethalMay be brought on by stress and/or exertionDelta wave is the slurring at the uptake of the QRS complex.
29 Junctional Tachycardia Often difficult to pick out so often identified as “SVT”
30 PJC’sFlat or inverted P Waveor P wave after the QRS
31 Ventricular Rhythms Originate in the ventricles / purkinje fibers Ventricular escape rhythm (idioventricular) rate 20-40Accelerated idioventricular rateVentricular tachycardia (VT) rate over 102Monomorphic – regular, similar shaped wide QRS complexesPolymorphic (i.e. Torsades de Pointes) – life threatening if sustained for more than a few seconds due to poor cardiac output from the tahchycardia)Ventricular fibrillation (VF)Fine & coarsePVC’s
38 R on T PVC’sTdP – Torsades de Pointes. QRS is wide, > 0.12 seconds, and bizarre with a rate often over 150 beats per minute.Long QT interval is measured as more than one half the R to R interval for that complex and the R wave following that complex.
39 R on T PVC’s cont. Why is R on T so bad? Downslope of T wave is the relative refractory periodSome cells have repolarized and can be stimulated again to depolarize/dischargeRelatively strong impulse can stimulate cells to conduct electrical impulses but usually in a slower, abnormal mannerCan result in ventricular fibrillationAbsolute refractory period is from the beginning of the QRS complex through approximately the first half of the T waveCells not repolarized and therefore cannot be stimulated
40 Synchronized Cardioversion Cardioversion is synchronized to avoid the refractory period of the T waveThe monitor “plots” out the next refractory period in order to shock at the right moment – the safe R waveWith a QRS complex & T wave present, the R wave can be predicted (cannot work in VF – no wave forms present)
41 A/V Heart Blocks 1st degree A condition of a rhythm, not a true rhythm Need to always state underlying rhythm2nd degreeType I - WenckebachType II – Classic – dangerous to the patientCan be variable (periodic) or have a set conduction ratio (ex. 2:1)3rd degree (Complete) – dangerous to the patient
42 Atrioventricular (AV) Blocks Delay or interruption in impulse conduction in AV node, bundle of His, or His/Purkinje systemClassified according to degree of block and site of blockPR interval is key in determining type of AV blockWidth of QRS determines site of block
43 AV Blocks cont. Clinical significance dependent on: Degree or severity of the blockRate of the escape pacemaker siteVentricular pacemaker site will be a slower heart rate than a junctional sitePatient’s response to that ventricular rateEvaluate level of consciousness / responsiveness & blood pressure
46 2nd Degree Type II (constant) P Wave PR Interval QRS CharacteristicsUniform Narrow & Uniform Missing QRS after every other P wave(2:1 conduction)Note: Ratio can be 3:1, 4:1, etc. The higher the ratio, the “sicker” the heart. (Ratio is P:QRS)
47 2nd Degree Type II (periodic) P Wave PR Interval QRS CharacteristicsUniform Narrow & Uniform Missing QRS after some P waves
50 Helpful Tips for AV Blocks Second degree Type IThink Type “I” drops “one”Wenckebach “winks” when it drops oneSecond degree Type IIThink 2:1 (knowing it can have variable block like 3:1, etc.)Third degree - completeThink completely no relationship between atria and ventricles
51 Implanted Pacemaker Most set on demand When the heart rate falls below a preset rate, the heart “demands” the pacemaker to take over51
53 Goal of Therapy Is rate too slow? Is rate too fast? Speed it up (Atropine, TCP)Is rate too fast?Slow it down (Vagal maneuvers, Adenosine, Verapamil)Blood pressure too low?Is there enough fluid (blood) in the tank?Improve contractility of the heart (dopamine, Epinephrine)Are the ventricles irritable?Soothe with antidysrhythmic (Amiodarone, Lidocaine)
54 Treatments for Rhythms As always… treat the patient NOT the monitorObtain baseline vitals before and/or during ECG monitoringIdentify rhythm and determine corresponding SOP to followHelpful to have at least one more person verify stripObtain patient history & OPQRST of current complaintOPQRST –O – onset (what were you doing at the time of onset?)P – provocation/palliation (what makes it worse; what makes it better?)Q – quality in the patient’s own wordsR – radiation to any where?S – severity measured on the 0-10 scaleT – what time did the symptoms start?
55 Transcutaneous Pacing No response to doses of atropineUnstable patient with a wide QRSSet pacing at a rate of 80 beats per minute in the demand modeStart output (mA) at lowest setting possible (0) and increase until capture notedSpike followed by QRS complexConsider medications to help with the chest discomfort
56 Tachycardias Can be generally well tolerated rhythms OR Can become lethal usually related to the heart rate and influence on cardiac outputAsk 2 questions:Is the patient stable or unstable?If unstable, needs cardioversionIf stable, determine if the QRS is narrow or wideQRS width drives decisions for therapy in stable patient
57 12-lead ECG Review Lead placement Lead II monitoringObtaining 12 lead EKGLead / location correlation of ST elevationST elevation criteria12 – lead practice EKG’s
58 12 Lead & Monitoring Lead Placement Einthoven’s TriangleArm and Leg leadsChest leads (V leads)Arm and leg leads may be placed on extremities or on the torso simulating right arm, left arm, right leg, and left leg.
59 Where do those chest stickers go? Make sure to “feel” for intercostal space – don’t just use your eyes!
60 ……and the FEMALES Bras loosened, people, if in your way Not all nipple lines are created equalCover the chest with a towel/sheet after leads are placed to preserve modesty
61 Lead Placement in the Female Avoid placing electrodes on top of breast tissueUse the back of the hand to displace breast tissue out of the way to place electrodeAvoids perception of “groping”Can ask the patient to move left breast out of way.
62 Lead PlacementThe more accurate the lead placement, the more accurate the 12-lead interpretation12-leads are often evaluated on a sequential basis, each interpretation considering the previous oneV4 - V6 should be in a gentle upward curve following the same 5th intercostal rib spaceCMC has done many trainingsWe should be doing this right by nowPlacement was standardized in 1938; this is proven science and placement must be accurate!
63 Heart & 12 – Lead Strip Correlation CX is the circumflex artery. Starts from the left descending artery and wraps around to the back of the heart.
64 12 – Lead Strips Remember: Every lead is like a “camera angle”
65 12 – Lead Strips cont. Imagine your strips broken into groups like this… aVRV4V1IIV5V2aVLIIIaVFV6V3
66 Remember… You will see Lead II first! This is how you monitor patient’s rhythmsMay see “reciprocal changes” as ST depression
67 Value of Reciprocal Changes* ST elevation means acute transmural injury – injury across all 3 layers of the heart muscleDiagnosis often based on:Presence of ST elevation in 2 or more contiguous leadsReciprocal changes*Confirms acute-injury patternsPatient historyPresentation
68 12 – Lead Comparison Chart for Reciprocal Change (Main ones are highlighted) Think 2 main limb leads reverse themselves for reciprocal changes: - II, III, aVF reciprocal for I and aVL - I and aVL reciprocal for II, III, aVF
69 Contiguous ECG LeadsEKG changes are significant when they are seen in at least two contiguous leadsTwo leads are contiguous if they look at the same area of the heart or they are numerically consecutive chest leads
70 ST Elevation Evaluation Locate the J-pointIdentify/estimate where the isoelectric line is noted to beCheck the standardized 2mm mark at the far left or beginning of each row of the EKG stripCompare the level of the ST segment 0.4 seconds after the J point to the isoelectric lineElevation (or depression) is significant if more than 1 mm (one small box) is seen in 2 or more leads facing the same anatomical area of the heart (ie: contiguous leads)Sensitivity measurement looks for >1mm elevation in contiguous leads. Specificity measures fro >2mm ST elevation in the chest (V) leads. Sensitivity will identify disease. Specificity may pick up less false-positives. In EMS, it is best to practice sensitivity than specificity in order to capture a broader number of potential patients and treat them as if they are having an acute MI rather than under treat and possibly miss an acute episode.
71 Measuring for ST Elevation Find the J pointIs the ST segment >1mm above the isoelectric line in 2 or more contiguous leads?
72 Complications of Lateral Wall MI I, aVL, V5, V6 Monitor for lethal heart blocksSecond degree type II – classicalThird degree heart block – completeTreat with TCPConsider sedation for patient comfortMonitor for captureMonitor for improvement by measuring level of consciousness and blood pressure
73 Complications of Inferior Wall MI II, III, aVF May see Mobitz type I – WenckebachDue to parasympathetic stimulation & not injury to conduction systemHypotensionRight ventricle may lose some pumping abilityVenous return exceeds output, blood accumulates in right ventricleLess blood being pumped to lungs to left ventricle and out to bodyDevelop hypotension, JVD, with clear lung soundsTreated with additional fluid administered cautiouslyContact Medical Control prior to NTG administrationBlood does not back up in the lungs; the right ventricle is not pumping well so there is no pulmonary edema from a right ventricular infarct (RVI).
74 Complications of Septal Wall MI V1 & V2 Monitor for lethal heart blocksSecond degree type II – classicalThird degree heart block – completeTreat with TCPRare to have a septal wall MI aloneOften associated with anterior and/or lateral wall involvement
75 Complications of Anterior Wall MI V3 & V4 Occlusion of left main coronary artery – the “widow maker”Cardiogenic shock and death without prompt reperfusionSecond degree AV block type IIOften symptomaticOften progress to 3rd degree heart blockPrepare to initiate TCPThird degree heart block – completeRhythm usually unstableRate usually less than 40 beats per minute
76 Acute Coronary Syndrome Routine Medical Care 12 Lead ECG and transmit, if availableStablePatient AlertSkin warm and drySystolic BP>100 mmHgAspirin 324 mg by mouthUnstableAltered Mental StatusSystolic BP< 100 mmHgAspirin 324 mg by mouth, if pt can tolerateContact Medical controlMonitor and TransportNitroglycerine 0.4 mg SLMay be repeated every 5 minIf pain persists following 2 doses, advance to Morphine SulfateMorphine Sulfate 2mg IVPSlowly over 2 minutesMay repeat every 2 minutes as needed, to a maximum total dose of 10 mgTransportNote: ASPIRIN my be withheld if patient is reliable and states has taken within 24 hours
77 Patient Presenting with Coronary Chest Pain – AMI Until Proven Otherwise OxygenMay limit ischemic injuryNew trends/guidelines coming out in 2011 SOP’sAspirin mg chewed (PO)Blocks platelet aggregation (clumping) to keep clot from getting biggerChewing breaks medication down faster & allows for quicker absorptionHold if patient allergic or for a reliable patient that states they have taken aspirin within last 24 hours
78 Acute Coronary Syndrome Medications cont. Nitroglycerin mg SL every minutesDilates coronary vessels to relieve vasospamsIncreases collateral blood flowDilates veins to reduce preload to reduce workload of heartWatch for hypotensionIf inferior wall MI (II, III, aVF), contact Medical Control prior to administrationIf pain persists after 2 doses, move to MorphineCheck for recent male enhancement drug use (ie: viagra, cialis, levitra)Side effect could be lethal hypotension
79 Acute Coronary Syndrome Medications cont. Morphine - 2 mg slow IVPDecreases pain & apprehensionMild venodilator & arterial dilatorReduces preload and afterloadGiven if pain level not changed after the 2nd dose of nitroglycerinGive 2mg slow IVP repeated every 2 minutes as neededMax total dose 10 mgPain level most likely will not be zero until the block has been removed and circulation has been restored.
80 Practice Rhythms Break into groups of 2 or 3 for rhythm quizzing Instructor will use wristwatch or stopwatch to give each group 30 seconds to determine stripYou don’t have 5 min in the field, you don’t get 5 min in the classroomMessage to Instructor:Refer to slide notes for more information
81 Sinus w/ 1st degree Block No symptoms are due to the first degree heart block; symptoms would be related to the underlying rhythm
82 Junctional Tachycardia Note: Inverted P waves; heart rate 140 How is the patient tolerating the heart rate?82
83 2nd Degree Type 1 – Wenckebach PR getting longer and finally 1 QRS drops; patient generally asymptomatic; can be normal rhythm for some patients
84 WPW Syndrome Slurring at beginning of QRS (delta wave) Better diagnosed on 12 lead EKG; patient asymptomatic unless heart rate becomes tachycardicNote presence of Delta Wave – slurring of beginning of the QRS complex84
85 2nd Degree Type II (2:1 conduction) Patient’s symptoms will be dependent on the heart rate – the slower the heart rate the more symptomatic the patient will be.2nd Degree Type II (2:1 conduction)Should be preparing the TCP for this patient
86 3rd degree heart block (complete) with narrow QRSSymptoms usually based on overall heart rate – the slower the heart rate the more symptomatic the patient. Prepare the TCP.
87 NSR to Torsade des Pointes If torsades is long lasting, patient may become unresponsive and arrest. Prepare for defibrillation followed immediately with CPR
88 Intermittent 2nd Degree Type II (Long PR intervals; periodic dropped beat)Consider need to apply TCP and then turn on if patient symptomatic
89 Why would this patient have symptoms of a stroke? Atrial fibrillation puts patient at risk from clots in the atria breaking loose and lodging in a vessel in the brainRhythm irregularly irregularPatient most likely on Coumadin and digoxin
90 Ventricular Tachycardia What 2 questions should you ask for all tachycardias?Is the patient stable or unstable?If stable, then you have time to determine if the QRS is narrow or wideWhat’s this strip?
91 Paroxysmal Supraventricular Tachycardia (PSVT) into sinus rhythm Evidence of abrupt stopping of the SVT
92 Sinus ArrhythmiaCommon in the pediatric patient and influenced by respirations. Treatment is not indicated
93 Sinus with unifocal PVC’s in trigeminy Often PVC’s go away after administration of oxygen
94 Multifocal Atrial Tachycardia (MAT) Rapid Wandering PacemakerIdentification can be SVT and treatment would be based on patient symptomsFocus on the P wave irregularity, not necessarily the name of the rhythm. Can be referred to as a rapid wandering pacemaker.94
95 12 – Lead Time! Same as Lead II strips Identify St elevation and try to give anatomical locationsRemember to be watchful for typical complications based on location of infarct and blocked coronary vessel
97 No ST elevation but peaked T waves (Hyperkalemia)
98 Hyperkalemia Can be caused by Over medication of potassium supplement (ex. K-dur)Excessive intake of foods (bananas are high in potassium)Crush syndromeAfter pressure/crush is released, the heart is hit with the potassium that built-up in the poorly perfused crushed areaToo much potassium can lead to critical heart dysrhythmias; difficult to treatOther populations at riskDialysis patientPatient in diabetic ketoacidosis
99 ST elevation in II, III & aVF (Inferior wall with LBBB) Watch for hypotension
100 ST Elevation Inferior Wall – II, III, aVF Watch for hypotension Reciprocal changes in I, aVL, V1, V2.
101 ST elevation in II, III, aVF (Inferior wall - note reciprocal changes) Watch for hypotension Reciprocal changes are ST depression seen in I and aVR if the ST elevation is in II, III, aVF.
102 ST elevation in V1 – V6, I & aVL (Anteroseptal with lateral extension) Extensive anteroseptal Watch for heart blockNote reciprocal changes of ST depression in II, III, and aVF.Serious infarct with high mortality rate (widow maker) due to occlusion high in the left anterior descending (LAD) coronary artery.
104 Documentation Rhythm strip interpretation If 12 lead EKG obtained: Note presence or absence of ST elevationIf ST elevation noted, in which leadsIf EKG was transmitted to hospital
105 Hospital Notification Notify the receiving hospital as soon as possible about a cardiac alertHow did you determine this may be a cardiac alert?Your general impression was made based on:Gathering patient historyPerforming a cardiac assessmentObtaining a 12 lead EKG as quickly as possible after first patient contact12 lead EKG evaluated for presence of ST elevationIt is not appropriate to wait until moving the patient to the ambulance before obtaining the 12 lead EKG. You may not be able to transmit the 12 lead until you have the patient and monitor back in the ambulance but you can obtain one and review where you first made contact with the patient.
106 Field TripIf your department can obtain lead EKG’s review the process for markingPatient age and raceYour department name on the 12 leadIf your department can fax, review the processGo to the ambulance to review the equipment and process
108 BibliographyAtwood, S., Stanton, C., Storey-Davenport, J. Introduction to Basic Cardiac Dysrhythmia 3rd Edition. MosbyJemsBledsoe, B., Porter, R., Cherry, R. Paramedic Care Principles & Practices Third Edition. BradyPage, B. 12 Lead ECG for Acute and Critical Care Providers. BradyPrevious CMC Cardiac CEsRegion X SOP March 2007; amended January 1, 2008Various webpagesFor pictures, rhythms, and graphsWalraven, G. Basic Arrhythmia 7th Edition. Brady