EKG REVIEW

Lead Placement

aVF

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Correlation of ECG Wave Forms .

III. and V5 and V6 . V4 • Anterior: V1–V4 • Anterolateral: V4–V6.EKG Distributions • Anteroseptal: V1. V2. III. V3. aVL • Lateral: I and aVL • Inferior: II. aVF. I. and aVF • Inferolateral: II.

Sistematika Membaca EKG •Rate •Ritme •Aksis •Interval •Infark •Hipertrof .

Sinus Rhythms • Originate in the SA node • • • • Normal sinus rhythm (NSR) Sinus bradycardia (SB) Sinus tachycardia (ST) Sinus arrhythmia • Inherent rate of 60 – 100 • Base all other rhythms on deviations from sinus rhythm .

Sinus Rhythm .

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Sinus Bradycardia .

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Sinus Tachycardia .

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Sinus Arrhythmia .

Marian Williams RN .

Atrial Rhythms • Originate in the atria • • • • • • • Atrial fbrillation (A Fib) Atrial flutter Wandering pacemaker Multifocal atrial tachycardia (MAT) Supraventricular tachycardia (SVT) PAC’s Wolff–Parkinson–White syndrome (WPW) .

A .Fib .

Flutter .A .

Wandering Pacemaker .

etc. • Often referred to as SVT by EMS • Recognize it is a tachycardia and QRS is narrow . intoxicated. acidotic.Multifocal Atrial Tachycardia (MAT) Pacemaker) •(Rapid SimilarWandering to wandering pacemaker (< 100) • MAT rate is >100 • Usually due to pulmonary issue • COPD • Hypoxia.

SVT .

PAC’s .

Preexcitation Syndrome) .Wolff–Parkinson–White (AKA .

AV/Junctional Rhythms • Originate in the AV node • • • • Junctional rhythm rate 40-60 Accelerated junctional rhythm rate 60-100 Junctional tachycardia rate over 100 PJC’s • Inherent rate of 40 .60 .

Junctional Rhythm .

Accelerated Junctional .

Junctional Tachycardia Often difficult to pick out so often identifed as “SVT” .

Torsades de Pointes) – life threatening if sustained for more than a few seconds due to poor cardiac output from the tahchycardia) • Ventricular fbrillation (VF) • Fine & coarse • PVC’s . similar shaped wide QRS complexes • Polymorphic (i.e.100 • Ventricular tachycardia (VT) rate over 102 • Monomorphic – regular.Ventricular Rhythms • Originate in the ventricles / purkinje fbers • Ventricular escape rhythm (idioventricular) rate 20-40 • Accelerated idioventricular rate 42 .

Idioventricular .

Accelerated Idioventricular .

VT (Monomorphic) .

VT (Polymorphic) Note the “twisting of the points” This rhythm pattern looks like Ribbon in it’s fluctuations .

VF .

PVC’s .

R on T PVC’s .

A/V Heart Blocks • 1st degree • A condition of a rhythm.Wenckebach • Type II – Classic – dangerous to the patient • Can be variable (periodic) or have a set conduction ratio (ex. 2:1) • 3rd degree (Complete) – dangerous to the patient . not a true rhythm • Need to always state underlying rhythm • 2nd degree • Type I .

1st Degree Block .

2nd Degree Type I .

12 . 4:1.20 QRS Narrow & Uniform Characteristics Missing QRS after every other P wave (2:1 conduction) Note: Ratio can be 3:1. (Ratio is P:QRS) . The higher the ratio. the “sicker” the heart.2nd Degree Type II (constant) P Wave PR Interval Uniform .. etc.

20 QRS Narrow & Uniform Characteristics Missing QRS after some P waves .2nd Degree Type II (periodic) P Wave PR Interval Uniform .12 ..

3rd Degree (Complete)

Sinus w/ 1st degree Block
No symptoms are due to the first degree heart
block; symptoms would be related to the
underlying rhythm

2nd Degree Type 1 – Wenckebach
PR getting longer and finally 1 QRS drops;
patient generally asymptomatic; can be
normal rhythm for some patients

2nd Degree Type II (2:1 conduction) Should be preparing the TCP for this patient .

3rd degree heart block (complete) with narrow QRS Symptoms usually based on overall heart rate – the slower the heart rate the more symptomatic the patient. Prepare the TCP. .

ST Elevation and non-ST Elevation MIs • When myocardial blood supply is abruptly reduced or cut off to a region of the heart. a sequence of events occur beginning with ischemia (inadequate tissue perfusion). followed by necrosis (infarction). and eventual fbrosis (scarring) if the blood supply isn't restored in an appropriate period of time. • The ECG changes over time with each of these events… .

ECG Changes Ways the ECG can change include: ST elevation & depression T-waves Appearance of pathologic Q-waves peaked inverted flattened .

or –Non-ST Elevation (Subendocardial or non-Q-wave) .ECG Changes & the Evolving MI There are two distinct patterns of ECG change depending if the infarction is: Non-ST Elevation ST Elevation –ST Elevation (Transmural or Q-wave).

peaked T-waves. then T-wave inversion Infarction ST elevation & appearance of Q-waves Fibrosis ST segments and T-waves return to normal.ST Elevation Infarction The ECG changes seen with a ST elevation infarction are: Before injury Normal ECG Ischemia ST depression. but Q-waves persist .

Ongoing infarction with appearance of pathologic Q-waves and T-wave inversion F. Fibrosis (months later) with persistent Q.waves. Ischemia from coronary artery occlusion results in ST depression (not shown) and peaked T-waves C.waves . Normal ECG prior to MI B. Infarction from ongoing ischemia results in marked ST elevation D/E. but normal ST segment and T.ST Elevation Infarction Here’s a diagram depicting an evolving infarction: A.

ST Elevation Infarction Here’s an ECG of an acute inferior wall MI: Look at the inferior leads (II. III. Question: What ECG changes do you see? ST elevation and Q-waves Extra credit: What is the rhythm? Atrial fibrillation (irregularly irregular with narrow QRS)! . aVF).

Q-waves and T-wave inversion .Non-ST Elevation Infarction Here’s an ECG of an inferior wall MI later in time: Now what do you see in the inferior leads? ST elevation.

but T-wave inversion persists .Non-ST Elevation Infarction The ECG changes seen with a non-ST elevation infarction are: Before injury Normal ECG Ischemia ST depression & T-wave inversion Infarction ST depression & T-wave inversion Fibrosis ST returns to baseline.

Non-ST Elevation Infarction Here’s an ECG of an evolving non-ST elevation MI: Note the ST depression and T-wave inversion in leads V2-V6. Question: What area of the heart is infarcting? Anterolateral .

12 – Lead Comparison Chart (Main ones are highlighted) .

ST elevation in V2 – V5 (Anterior wall) .

ST elevation in II. III & aVF (Inferior wall with LBBB) .

III.ST Elevation Inferior Wall – II. aVF .

III.ST elevation in II. aVF (Inferior wall .note reciprocal changes) Watch for hypotension .

ST elevation in V1 – V6. I & aVL (Anteroseptal with lateral extension) Extensive anteroseptal Watch for heart block .

ST elevation V2-V5 Watch for heart block .

Left Ventricular Hypertrophy .

What stands out as different with the second one? Normal Left Ventricular Hypertrophy Answer: The QRS complexes are very tall (increased voltage) .Left Ventricular Hypertrophy Compare these two 12-lead ECGs.

Left Ventricular Hypertrophy Why is left ventricular hypertrophy characterized by tall QRS complexes? As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage. LVH Increased QRS voltage ECHOcardiogram .

However for now. . • For example: • The R wave in V5 or V6 plus the S wave in V1 or V2 exceeds 35 mm. all you need to know is that the QRS voltage increases with LVH.Left Ventricular Hypertrophy • Specifc criteria exists to diagnose LVH using a 12-lead ECG.

. This is his ECG.SUMMARY Rate Rhythm Axis Intervals Hypertrophy Infarct A 16 yo young man ran into a guardrail while riding a motorcycle. In the ED he is comatose and dyspneic.

SUMMARY Rate Rhythm Axis Intervals Hypertrophy Infarct What is the rate? Approx. 132 bpm (22 R waves x 6) .

SUMMARY Rate Rhythm Axis Intervals Hypertrophy Infarct What is the rhythm? Sinus tachycardia .

SUMMARY Rate Rhythm Axis Intervals Hypertrophy Infarct What is the QRS axis? Right axis deviation (.in I. + in II) .

08 s. QRS = 0. QTc = 0.482 s and QT intervals? . QRS PR = 0.12 s.SUMMARY Rate Rhythm Axis Intervals Hypertrophy Infarct What are the PR.

notched or negatively deflected P waves) .SUMMARY Rate Rhythm Axis Intervals Hypertrophy Infarct Is there evidence of atrial enlargement? No (no peaked.

SUMMARY Rate Rhythm Axis Intervals Hypertrophy Infarct Is there evidence of No (no tall R waves in V1/V2 or V5/V6) ventricular hypertrophy? .

SUMMARY Rate Rhythm Axis Intervals Hypertrophy Infarct Infarct: Are there abnormal Q waves? 30 30 30 30 Yes! In leads V1-V6 and I. avL Any R40 20 Any R50 30 Any 30 .

.SUMMARY Rate Rhythm Axis Intervals Hypertrophy Infarct Infarct: Is the ST elevation or depression? Yes! Elevation in V2-V6. III and avF. Depression in II. I and avL.

SUMMARY Rate Rhythm Axis Intervals Hypertrophy Infarct Infarct: Are there T wave changes? No .

avL) with reciprocal changes (the ST depression) in the inferior leads (II. An angiogram showed total occlusion in the proximal LAD with collaterals from the RCA and LCX. I. III. This young man suffered an acute myocardial infarction after blunt trauma. long QT. .SUMMARY Rate Rhythm Axis Intervals Hypertrophy Infarct ECG analysis: Sinus tachycardia at 132 bpm. avF). right axis deviation. An echocardiogram showed anteroseptal akinesia in the left ventricle with severely depressed LV function (EF=28%). and evidence of ST elevation infarction in the anterolateral leads (V1-V6.

End of Module VII b Reading 12-Lead ECGs Proceed to Module VII b Practice Quiz on your iROCKET Course .