CMC EMS System ECRN CE 12 Lead EKG’s

Mod I 2009 CE Prepared by: Sharon Hopkins, RN, BSN

Objectives

 Upon successful completion of this module, the ECRN will be able to accomplish the following:  Identify the appropriate components of the cardiac conduction system with the correct wave form on a rhythm strip.

  Identify when it is appropriate to obtain an EKG Identify the criteria for significant ST elevation.

 Identify EKG leads that view the anterior, inferior, lateral walls, and septum

Objectives

   Recognize the patterns of an MI after viewing the components of a 12 lead EKG    Identify typical and atypical presentations of AMI Identify complications associated with an inferior wall MI Identify complications associated with an anterior/septal wall MI Identify complications associated with a lateral wall MI Identify interventions for complications related to heart block, pulmonary edema, and cardiogenic shock  Identify the SOP guidelines for the patient presenting with acute coronary syndrome as written in the Region X SOP’s

Objectives

 State dosing and precautions for Aspirin, Nitroglycerin, and Morphine in the Region X SOP’s.

 Identify ED staff expectations of EMS personnel when calling the hospital to report a patient with ST elevation identified on a 12 lead EKG  Identify EMS expectations when delivering a patient to a hospital after ST elevation has been identified on a 12 lead EKG  Given a picture, correctly trace the order of the cardiac conduction system.

 Given a picture, correctly identify electrode placement to obtain a 12 lead EKG.

Why Are We doing Pre-hospital EKG’s?

 Early recognition and fast, appropriate treatment can prevent the extension of an MI  Early recognition = early intervention  An important diagnostic tool will also be the patient’s general appearance

Cardiac Conduction System

 Electrical cells arranged in a systematic pathway  Predominant pacemaker starting the electrical flow comes from the SA node  Electrical cells are part of the conduction system  Muscle cells are the mechanical cells

Cardiac Conduction System

1 2 4 3 Purkinje fibers 5 4

EKG Waveforms

   P wave represents atrial stimulation  P wave is rounded and upright PR interval  Includes the P wave and the isoelectric PR segment  PR interval is the time it takes for an impulse to travel from the SA node through the internodal pathways toward the ventricles  Includes delay time in the AV node Normal PR interval is 0.12 – 0.20 seconds

PR Interval Normal 0.12 – 0.20 seconds

PR Interval Abnormalities

 PR interval <0.12 seconds  Impulse did not begin in the normal pacemaker site of the SA node but somewhere in the atria  PR interval >0.20 seconds  There was a longer than normal delay transmitting the impulse through the AV node  A change in the PR interval measurement generally will not make the patient symptomatic

EKG Wave Forms cont’d

   QRS complex  Consists of the Q, R, and S waves collectively  Represents ventricular depolarization or discharge of electrical energy throughout ventricular muscle  Larger than the P wave because ventricular depolarization involves a larger muscle mass than atrial depolarization Palpation of a pulse is generated by ventricular depolarization (seen as the QRS complex) Normal timing usually considered between 0.06 and 0.11 seconds  Normal is less than 0.12 seconds

QRS Complex

QRS

QRS Complex Measurement

   From beginning of Q wave – usually fairly straight forward  Stop measurement at end of S wave; not necessarily where QRS intersects baseline  On S wave, watch for small notch or other indicator that electrical flow is changing  Not always so easy to determine stop point Do not include ST segment or T wave Abnormally wide QRS indicates delay in conduction time through the ventricles

EKG Wave Forms cont’d

 T wave  Represents ventricular repolarization  Repolarization is the phase of electrical activity where electrical charges (influenced primarily by sodium (Na+) and potassium (K+)) return to their original state and prepare to respond to the next electrical charge received  Atria repolarize during ventricular depolarization so the small atrial T wave is hidden during the larger QRS complex

When To Obtain a 12-Lead EKG

 Any patient presenting with signs and/or symptoms of an acute coronary syndrome  Consider atypical AMI presentations  Elderly  Women  Patient with long standing history of diabetes  Any patient presenting with a Second degree Type II (classical) or 3 rd degree heart block  Consider the origin of heart block from an AMI until proven otherwise

What Are We Looking For?

 Abnormalities that indicate interruption in the blood flow to the myocardium  Plaque formation diminishes blood flow through the coronary arteries  Patients may be asymptomatic while damage silently develops  Plaque rupture begins a cascade of events that further compromises blood flow through the injured vessel(s)  This cascade of events could lead to an acute coronary syndrome (ie: acute MI)

Coronary Circulation

  Coronary arteries and veins Myocardium extracts the largest amount of oxygen as blood moves into general circulation  Oxygen uptake by the myocardium can only improve by increasing blood flow through the coronary arteries  If the coronary arteries are blocked, they must be reopened if circulation is going to be restored to that area of tissue supplied

12-Lead Electrodes

 A lead is a tracing of the electrical activity between 2 electrodes  Leads view the heart from the front of the body  Top, bottom, right, and left side of heart  Leads view the heart as if it were sliced in half horizontally  Front, back, right, and left sides of heart  Each lead has a positive and a negative electrode

Standard 12-Lead EKG

 Six limb leads  Leads I, II, III, aVR, aVL, aVF  Six chest leads (precordial leads)  V1, V2, V3, V4, V5, V6  Information from 12 leads obtained from the attachment of only 10 electrodes

View The Leads Provide

   II, III, aVF – view inferior wall of heart V1 and V2 – view septal wall of heart V3 and V4 – view anterior wall of heart  I, aVL, V5, V6 – view lateral wall of heart

Preparation for 12 Lead EKG

 Skin preparation  Hair removal  clip hair if necessary so electrodes adhere  Clean and dry skin surface  gently rub skin area with gauze pad  need to remove skin oils & dead skin  if diaphoretic patient wipe with towel/gauze or use antiperspirant spray

 Patient positioning  Preferably flat  Heart rotates position as the patient position changes  If patient is elevated, note that information on the EKG

Precordial Chest Leads

For every person, each precordial lead placed in the same relative position  V1 - 4 th  V2 - 4 th intercostal space, R of sternum intercostal space, L of sternum  V4 - 5 th intercostal space, midclavicular  V3 - between V2 and V4, on 5 th rib  V5 - 5 th  V6 - 5 th intercostal space, anterior axillary line intercostal space, mid-axillary line

2nd ICS 3rd ICS 1st ICS  Precordial leads

12 Lead EKG Printout

  Standard format 8 1 / 2  x 11  paper 12 lead format: I aVR V1 V4 II III aVL aVF V2 V3 V5 V6

Machines can analyze data obtained but humans must interpret data

II

I III aVR aVL aVF V1 V2 V3 V4 V5 V6

Lateral View – I, aVL, V5, V6

I aVL V5 V6

Inferior View – II, III, aVF

III II aVF

Septal View – V1 & V2

V1 V2

Anterior View – V3 & V4

V4 V3

Myocardial Insult

 Ischemia  lack of oxygenation   ST depression or T wave inversion permanent damage avoidable  Injury   prolonged ischemia ST elevation  permanent damage avoidable  Infarct  death of myocardial tissue; damage permanent; may have Q wave

Why A Pre-hospital EKG?

  EMS looking for ST segment elevation  Indicates injury that can be reversible if found early and acted upon early   TIME IS MUSCLE The earlier the discovery of an acute cardiac event, the quicker the patient can receive the most appropriate care EKG’s sent to the ED before patient arrival allows for the right personnel to be available to properly care for the patient in the most time efficient manner

What Does EMS Have to Do?

  Obtain a 12 lead EKG EMS to evaluate the leads as they are sending the 12 lead to the ED  Identify for the presence or absence of ST elevation  EMS to report what they see, not just what is printed on the machine copy of the EKG  Upon arrival, EMS to hand a copy of their 12 lead to the ED staff while they give bedside report

Evaluating for ST Segment Elevation

  Locate the J-point Identify/estimate where the isoelectric line is noted to be  Compare the level of the ST segment to the isoelectric line  Elevation (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-see slide #41, #42)

The J Point

 J point – where the QRS complex and ST segment meet  ST segment elevation - evaluated 0.04 seconds (one small box) after J point

 Coved shape usually indicates acute injury  Concave shape is usually benign especially if patient is asympto matic

Significant ST Elevation

 ST segment elevation measurement  starts 0.04 seconds after J point  ST elevation  > 1mm (1 small box) in 2 or more contiguous chest leads (V1-V6)  >1mm (1 small box) in 2 or more anatomically contiguous leads (ie: II, III, aVF; I, aVL, V5, V6)  Contiguous lead  limb leads that “look” at the same area of the heart or are numerically consecutive chest leads (ie: V1 – V6)

Contiguous Leads

     Lateral wall: I, aVL, V5, V6 Inferior wall: II, III, avF Septum: V1 and V2 Anterior wall: V3 and V4 Posterior wall: V7-V9 (leads placed on the patient’s back 5 th intercostal space creating a 15 lead EKG)

Evolution of AMI A - pre-infarct (normal) B - Tall T wave (

first few minutes of infarct

) C - Tall T wave and ST elevation (

injury

) D - Elevated ST (

injury

), inverted T wave (

ischemia

), Q wave (

tissue death

) E - Inverted T wave (

ischemia

), Q wave (

tissue death

) F - Q wave (

permanent marking)

ST Segment Elevation

EKG monitoring  Evaluates electrical activity of the heart  Can indicate myocardial insult and location  ischemia - initial insult; ST depression seen  injury - prolonged myocardial hypoxia or ischemia; ST elevation seen  infarction - tissue death  dead tissue no longer contracts  amount of dead tissue directly relates to degree of muscle impairment  may show Q waves

Contiguous ECG Leads

 EKG changes are significant when they are seen in at least two

contiguous

leads  Two leads are contiguous if they look at the same area of the heart or they are numerically consecutive chest leads

Groups of EKG Leads

    Inferior wall - II, III, aVF Septal wall - V1, V2 Anterior wall - V3, V4 Lateral wall - I, aVL, V5, V6   aVR is not evaluated in typical groups Standard lead placement does not look at posterior wall or right ventricle of the heart need special lead placement for these views

Basic 12-Lead EKG Format

Lead I Lateral wall aVR not evaluated V 1 Septum V 4 Anterior wall Lead II Inferior wall aVL Lateral wall Lead III Inferior wall aVF Inferior wall V 2 Septum V 5 Lateral wall V 3 Anterior V 6 Lateral wall

Lateral Wall MI: I, aVL, V5, V6

Source: The 12-Lead ECG in Acute Coronary Syndromes, MosbyJems, 2006.

Inferior Wall MI II, III, aVF

Source: The 12-Lead ECG in Acute Coronary Syndromes, MosbyJems, 2006.

Septal MI: Leads V1 and V2

Source: The 12-Lead ECG in Acute Coronary Syndromes, MosbyJems, 2006.

Anterior Wall MI V3, V4

Source: The 12-Lead ECG in Acute Coronary Syndromes, MosbyJems, 2006.

Posterior MI – Reciprocal Changes ST Depression V1, V2, V3, poss V4

Source: The 12-Lead ECG in Acute Coronary Syndromes, MosbyJems, 2006.

Complications of Lateral Wall MI

 I, aVL, V5,V6  Complications arise due to the conduction components that are in the septum  Conduction dysrhythmias most common    Second degree Type II – classical 3 rd degree – complete heart block Bundle branch blocks  Monitor patient closely for these blocks  2 nd degree Type II and 3 rd degree are serious dysrhythmias that need to be treated aggressively with TCP

Complications of Inferior Wall MI

 II, III, aVF  40% of patients with inferior MI’s have right ventricular infarcts  In the presence of a right ventricular infarct, there is a high likeliness of both ventricles being damaged  Contraction capabilities will be negatively affected   Patients may present hypotensive Nitrates and Morphine alone will dilate blood vessels worsening hypotension  Under Medical Control direction patients are often treated with a fluid challenge with the nitrates  1 st degree heart block and Second degree Type I Wenckebach most common heart blocks

Complications of Septal Wall MI

     V1 and V2 Significant amount of conduction components are in the septal area Patient predisposed to dysrhythmia  Second degree Type II – classical   3 rd degree heart block Bundle branch block Lethal heart blocks treated aggressively - TCP Rare to have a septal MI alone  Common to have anterior or lateral involvement along with septal area

Complications of Anterior Wall MI

     V3, V4 Known as the “widowmaker” due to the potential for a massive area of infarction from blockage of the large amount of myocardium supplied by the LAD (left anterior descending artery) Often the septal or lateral walls are also involved Watch for lethal ventricular dysrhythmias and cardiogenic shock Second degree Type II and 3 rd degree heart block are more common than other blocks

Anterior Wall MI - V3, V4

 Early death within a few days often from CHF  Massive area of ventricular tissue infarcted if LAD totally occluded  Important to obtain history of recent MI diagnosis and hospital discharge  Increased incidence of ventricular tachycardia (VT) and ventricular fibrillation (VF) up to 1 -2 weeks post acute anterior MI

Additional Complications

 Acute pulmonary edema  Nitroglycerin given to dilate blood vessels and reduce preload  Lasix given to dilate blood vessels and reduce preload; as a diuretic  Morphine given to dilate blood vessels and reduce preload; reduce anxiety  All medications and interventions (ie: CPAP) can drop the B/P – monitor carefully

Additional Complications

 Cardiogenic shock    Ineffective pumping from the damaged heart IV fluid challenge if lung sounds are clear Dopamine drip titrated to maintain a systolic blood pressure of >100 mmHg  Start at a low dose (5mcg/kg/min)  Estimate the patient’s pounds (ie: 100 #)  Take the 1 st 2 numbers dropping the last number (“10”)  Minus 2 from the 1 st 2 numbers  This is the starting point for minidrips/minute (10 – 2 = 8 minidrips/minute)

Common Terms Patients Use To Describe Chest Pain

 Heaviness  Burning  Pressing  Constricting band  Suffocating  Squeezing  Strangling  A weight in the center of my chest  A vise tightening around my chest

Additional Patient Complaints or Presentations

 Difficulty breathing  Excessive sweating  Unexplained nausea or vomiting  Generalized weakness  Dizziness  Syncope or near syncope  Palpitations  Isolated arm or jaw pain  Fatigue  Dysrhythmias

Typical Injury Patterns

Source: The 12-Lead ECG in Acute Coronary Syndromes, MosbyJems, 2006.

Atypical Presentation in the Elderly

 Most frequent symptoms of acute MI:  Shortness of breath  Fatigue and weakness (“I just don’t feel well”)  Abdominal or epigastric discomfort  Often have preexisting conditions making this an already vulnerable population  Hypertension  CHF  Previous AMI  Likely to delay seeking treatment

Atypical Presentation in Women

 Discomfort described as:  Aching  Tightness  Pressure  Sharpness  Burning  Fullness  Tingling  Frequent acute symptoms:  Shortness of breath  Weakness  Unusual fatigue  Cold sweats  Dizziness  Nausea/vomiting Often have no actual chest pain to offer as a complaint. Often the pain is in the back, shoulders, or neck

Atypical Presentation in the Patient With Diabetes

 Atypical presentation due to autonomic dysfunction  Common signs/symptoms:      Generalized weakness Generalized feeling of not being well Syncope Lightheadedness Change in mental status

Region X SOP – Acute Coronary Syndrome

 A 12 lead EKG is obtained on all patients presenting with signs and symptoms of acute MI OR  For patients where suspicions are raised that the patient may be experiencing an acute MI (ie: heart block)

12-Lead Electrode Placement

Region X SOP – Acute Coronary Syndrome

 Determine if the patient is stable or unstable to proceed with interventions  Easiest way to determine stability is to evaluate blood flow  What is the level of consciousness?

 What is the blood pressure / is there a radial pulse?

 Remember: A B/P reading of 100/systolic does not necessarily indicate the presence or absence of symptoms

Oxygen

   Provide what the patient needs Evaluate each individual clinical presentation  In the presence of an acute MI, the myocardium is being deprived of blood flow and therefore adequate oxygen levels All patients deserve some form of oxygen in this early period of myocardial starvation for it

Aspirin

   Used to prevent platelet aggregation  When a plague ruptures, chemicals are released. Platelets congregate to the area to seal the rupture. Platelet aggregation further increases the degree of vessel blockage.

Field dosage is 4 – 81 mg (324 mg total) baby aspirin chewed  Chewing breaks down the aspirin and allows for faster absorption Give dose if patient not reliable about taking their own dose or has not taken any aspirin

Nitroglycerin

 Venodilator  Improves coronary blood flow  By dilating blood vessels, pools blood away from the heart which decreases preload. This decreases the work load of a stressed heart.

 Carefully monitor blood pressure before and after dosages  Field dosage is 0.4 mg tablet sl   Dosage can be repeated in 5 minutes if blood pressure remains stable FYI: Pain level will not drop to “0” until the clot is removed

For CMC EMS System Participants

  There should be no delay in obtaining a 12 lead EKG in the field and transmitting it to the ED  If the patient is <35 years of age  Follow Acute coronary Syndrome SOP by administering aspirin  Medical Control contacted prior to administration of nitroglycerin or morphine A visual interpretation is to be given during report to the receiving hospital even when the 12 lead EKG is faxed in

Morphine

  CNS depressant to reduce anxiety Venodilates blood vessels to reduce the volume of blood returning to the heart to decrease the heart’s workload  Field dosage is 2 mg slow IVP  Dosage started when the 2 nd dose of nitroglycerin proves ineffective  Dosage may be repeated every 2 minutes as needed  Maximum dosage is 10 mg  Watch for hypotension

Receiving Hospital Report

 When sending a 12 lead EKG, EMS to inform the receiving hospital what identifiers have been used     Department ID number Patient sex (M / F) Patient age Any other identifier  EMS should always give their visual interpretation of what they have observed for ST elevation

Activating a Cardiac Alert

   The ED activates a cardiac alert to prepare the cardiac team to provide optimal care for the patient Typical cardiac alert team members       ED staff – MD, RN, tech, secretary Cardiologist Cath lab personnel EKG tech (may be an ED staff member) Lab tech X-ray tech Not all hospitals use all members in a formalized team but all of these members are somehow integrated into the care of the patient

When Does a Cardiac Alert Get Called?

 When EMS sends a 12 lead EKG with ST elevation, the team gets activated  When EMS confirms what they see on the 12 lead, whether the EKG is sent or not, may trigger a cardiac alert  There is a direct link in EMS accuracy, completeness in patient report, and EKG interpretation with pre-hospital activation of the cardiac alert team

Transferring Care of The Patient to The ED

 Bedside report is restated to the ED personnel in the room  The main report must be to an RN or MD  Rhythm strips and 12 lead EKG are presented  Important to note positive and negative changes in the patient condition   Pain level has decreased Blood pressure has dropped

EKG Practice

 Practice reviewing the following 12 lead EKG’s for ST segment elevation   Evaluate the ST segment at the J point Note: A peaked T wave is not equivalent with ST elevation  Consider potential complications to monitor for based on the location of the acute MI  Vignette follows the 12 lead EKG picture

Practice Identifying ST Segment Elevation

> 1mm (1 small box) above the baseline in 2 leads from any group or 2 or more contiguous leads (>2 mm (2 small boxes) in limb leads considered alternative elevation by some) measured 0.04 seconds after J point

Case #1

Case #1

   52 year-old patient complains of indigestion after pizza & beer dinner.

VS: 124/82; P – 108; R - 18 Is there ST elevation:     I, aVL, V5, V6?

II, III, aVF?

V1, V2?

V3, V4?

  What are you going to do for this patient?

(There is no ST elevation)

Case #2

Case #2

     62 year-old female developed chest & jaw pain while in the shower VS: 110/62; P – 66; R – 20 Is there ST elevation:     I, aVL, V5, V6?

II, III, aVF?

V1, V2?

V3, V4?

What are you going to do for this patient?

(ST elevation II, III, aVF – Inferior wall MI)

Case #3

Case #3

     45 year-old patient who complains of chest heaviness & lightheadedness VS: 90/56; P – 86; R - 22 Is there ST elevation:     I, aVL, V5, V6?

II, III, aVF?

V1, V2?

V3, V4?

What are you going to do for this patient?

(ST elevation V2-V5 – anterior infarction)

Case #4

Case #4

     87 year-old female patient complains of dizziness and being extremely tired VS: 88/52; P – 30; R - 16 Is there ST elevation:     I, aVL, V5, V6?

II, III, aVF?

V1, V2?

V3, V4?

What are you going to do for this patient?

(ST elevation II, III, aVF, V2-V4)

Case #5

Case #5

     58 year-old male patient who complains of chest pain radiating down the left arm after working out in the gym VS: 110/72; P – 100; R - 18 Is there ST elevation:  I, aVL, V5, V6?

   II, III, aVF?

V1, V2?

V3, V4?

What are you going to do for this patient?

(ST elevation II, III, aVF)

Case #6

Case #6

     92 year-old patient complaining of pounding in her chest for one hour VS: 98/66; P – 110; R- 16 Is there ST elevation:     I, aVL, V5, V6?

II, III, aVF?

V1, V2?

V3, V4?

What are you going to do for this patient?

(ST elevation V1-V4 – anterioseptal MI)

Case #7

Case #7

 66 year-old patient with history of diabetes for 25 years complains of being lightheaded and is sweaty  Is there ST elevation:  I, aVL, V5, V6?

  II, III, aVF?

V1, V2?

 V3, V4?

  What are you going to do for this patient?

(Normal EKG – sinus bradycardia)

Case #8

Case #8

   70 year-old patient had a syncopal episode when they stood up from the couch VS: 156/98; P – 76; R - 16 Is there ST elevation:     I, aVL, V5, V6?

II, III, aVF?

V1, V2?

V3, V4?

  What are you going to do for this patient?

(ST elevation V2, V3, slightly in V1, V4)

Case #9

Case #9

     82 year-old patient complains of sudden onset of slurred speech, inability to grasp a coffee cup, and inability to follow simple commands VS: 122/84; P – 110; R - 18 Is there ST elevation:  I, aVL, V5, V6?

   II, III, aVF?

V1, V2?

V3, V4?

What are you going to do for this patient?

(No ST elevation, atrial fibrillation rhythm)

Case #10

Case #10

     36 year-old patient who passed out standing in line at a bank VS: 128/78; P – 80; R - 20 Is there ST elevation:     I, aVL, V5, V6?

II, III, aVF?

V1, V2?

V3, V4?

What are you going to do for this patient?

(ST elevation II, III, aVF)

 

Bibliography

Aehlert, B. EKG’s Made Easy third Edition. Elsevier Mosby. 2006.

Beasley, B. Understanding EKG’s A Practical Approach. Brady. 2003.

 Bledsoe, B., Porter, R., Cherry, R. Paramedic Care Principles and Practices. Third Edition. Brady. 2009.

 Ellis, K. EKG Plain and Simple. Prentice Hall. 2002.

 Page, B. 12 Lead EKG for Acute and Critical Care Providers. Brady. 2005.

  Phalen, T., Aehlert, B. The 12 Lead EKG in Acute Coronary Syndromes. Second Edition, Elsevier Mosby. 2006.

Region X SOP’s. March 2007, Amended January 1, 2008.

  freemd.com (Acute Coronary Syndrome 9/2008) www.anaesthetist.com/icu/organs/heart/ecg/Find ex.htm

  www.ecglibrary.com/ www.gwc.maricopa.edu/class/bio202/cyberheart /ekgqzr.htm

 www.madsci.com/manu/ekg_mi.htm