ecg workshop - snapup tickets · 2016. 11. 9. · ecg workshop university health network emergency...

ECG Workshop

University Health Network

Emergency Medicine Conference 2016

Shirley Strachan-Jackman NP, MN, ENC(C)

Objectives

• Discuss the approach to the patient with chest pain

• Review heart blocks

• Take a step-by-step approach to ECG interpretation

• Identify normal and abnormal components on the ECG

• Determine how a 12/15 lead helps diagnose pathological conditions

• Identify EGC changes for ischemia, AMI, BBB, pericarditis, PE, LVH, and electrolyte imbalances

Most Importantly.....

• Have fun—and next time you take an ECG for a physician sign-off, you will be able to tell them what’s normal or abnormal...he or she will be impressed!

Chest pain is merely a symptom, not a diagnosis

Differential Diagnosis of Chest Pain

• Cardiac causes- CAD, stable angina, unstable angina, variant angina, STEMI, NSTEMI

• Pericarditis

• Valvular diseases- aortic stenosis, subaortic stenosis, mitral valuve prolapse

• Vascular causes- aortic dissection, PE, pulmonary hypertension

• Pulmonary causes- pleural irritation d/t infection, inflammation, infiltration, pneumothorax, tracheobronchitis

• MSK- costochondritis, muscle strain, cervical/thoracic spine problems

• GI causes- esophageal reflux/spasm, biliary colic, peptic ulcer disease, pancreatitis

• Miscellaneous causes-herpes zoster, chest wall tumours, anxiety

It’s not always a textbook presentation

• People who present with right-sided chest pain—50% AMI

• Elderly—cognitive impairment—be aware of fatigue, weakness, dizziness, NFW, SOB

• Diabetics—neuropathy, often do not have pain

Our goal is to…

• Identify those patients with life-threatening etiologies

- Aortic Dissection

- Myocardial Infarction

- Unstable Angina

- Massive PE

- Cardiac Tamponade

ECG…

…is the best single test available in the ED

…history is important with the physical examination

Conduction System

Pacemaker Rates

Lead Placement

• Lead placement is important—inaccurate placement of > 3/5 inch- can lead to inaccurate waveforms and an incorrect ECG interpretation

15 Lead Electrode Placement

Components of the ECG Complex

Pathological Q-Wave

ST Segment Depression

Injury- ST Elevation

QT Interval

Normal Coronary Arteries

RCA

- Inferior wall of LV - Posterior wall of LV - Right ventricle - Sinus node (55%) - AV node (85%)

LCA - Lateral wall LV

- SA node (45%)

- AV node (15%)

- Posterior division of the left branch

LADA

- Anterior wall of LV

- Anterior portion of the septum

- Right bundle branch

- Anterior division of left branch

Limb Leads vs. Chest Leads

• Limb leads- I, II, III, AVR, AVL, AVF

View the heart on the vertical plane- from the sides, above and below

• Chest leads- V1 to V6

View the heart on the horizontal plane- from the front and left side

Each lead views the heart at a unique angle

Heart Blocks

• First degree AVB

• Second degree AVB Type I; Mobitz I; Wenckebach

• Second degree AVB Type II; Mobitz II

• Third degree AVB; Complete Heart Block

First Degree AV Block

Second Degree AV Block Type I

• Each successive impulse from the SA node is delayed slightly longer than the previous impulse until the impulse fails to be conducted to the ventricles- and the cycle repeats itself. Think of… longer, longer, drop.

• Causes- CAD, Inferior wall MI and rheumatic fever; as well as cardiac medications such as digoxin, Inderal, verapamil

Second Degree AV Block Type I

Second Degree AV Block Type II

• Less common than type I but more serious- ventricular rate is slower and cardiac output diminished- more likely to cause symptoms

• Generally caused from a anterior-wall MI, degenerative changes in the conduction system or severe CAD

• Strip will look like someone erased some QRS complexes- the PR interval will always be constant before the QRS complexes

• QRS complexes may be wide

Second Degree AV Block Type II

Third Degree AV Block

• Impulses are completely blocked at the AV node and can’t be conducted to the ventricles

• Potentially life-threatening

• Atria and ventricles act independently

– If block is right at the AV node- HR 40-60- QRS narrow

– If block is Purkinje system- HR < 40- QRS wide

Third Degree AV Block

Figuring it all out! Block Teams

Constant/ Fixed P wave Varied P wave

First Degree AVB

Second Degree AVB Type II

Second Degree AVB Type I

Third degree AVB

Think of Heart Blocks Like a Marriage

Ten Rules to a Normal ECG

Which Each Lead “Sees”

Lateral Septal/ Anterior

Anterior

Lateral Lateral

Lateral

Inferior

Inferior Inferior Anterior

Septal/ Anterior

Rule # 1

PR interval should be 3-5 small squares

Rule # 2

The width of the QRS complex is less than 3 small squares

Rule # 3

The QRS complex should be dominantly upright in leads I and II

Rule # 4

The QRS and T waves tend to have the same general direction in the limb leads

Rule # 5

All waves are negative in lead aVR

Rule # 6

The R wave in the precordial leads must grow from V1 to at least V4

Rule # 7

ST segment should be isoelectric

Rule # 8

P waves should be upright in leads I, II and V2-V6

Rule # 9

There should be no Q wave or a small Q wave (less than 0.04 secs. in width) in leads I, II and V2-V6

Rule # 10

T waves must be upright in leads I, II and V2-V6

ECG Approach

1. Assess heart rate and rhythm.

2. Determine electrical axis.

3. Examine R wave progression—normally the R wave gets taller from V1 to V4—gets slightly smaller in V6 (no R wave progression-??MI).

4. Check for ischemia or infarction pattern: Check inferior leads/ posterior leads

Check lateral leads

Check anterior leads

If needed, check right ventricular leads

Check V1 for RBBB & LBBB

Electrical Axis

Factors that influence electrical axis include:

position of heart

person’s body size and type

conduction pathways

force of the electrical impulse being generated

Electrical Axis

Causes of Left Axis Deviation

• Normal deviation

• Inferior wall MI

• Left anterior hemiblock

• Wolff-Parkinson-White Syndrome

• Mechanical shifts—pregnancy, ascites, tumors

• LBBB

• Left ventricular hypertrophy

• Aging

Causes of Right Axis Deviation

• Normal deviation

• Lateral wall MI

• Left posterior hemiblock

• RBBB

• Emphysema

• Right ventricular hypertrophy

Early Repolarization

• Produces an infarct-like pattern of healthy, asymptomatic patients

• ST-segment elevation is seen

• Produces tall T-waves

Early Repolarization

Bundle Branch Blocks

• BBB is caused by a block of the impulse of the right or left bundle branch

• Complete or incomplete

• Normally, the RBB quickly transmits the stimulus of depolarization to the right ventricle. The LBBB does the same to the left ventricle. This stimulus is transmitted to both ventricles at the same time.

Right Bundle Branch Block (RBBB)

• In RBBB, the initial impulse activates the interventricular septum from the left to right, just as in normal activation

• The LBB activates the left ventricle—the impulse then crosses the interventricular septum to activate the right ventricle—the right ventricle fires late

RBBB ECG Features

• Best seen in V1

• QRS complex > or = to .12 seconds

• QRS predominantly positive in V1

• Other features include slurred S wave in lateral leads

RBBB

How LBBB occurs

• In LBBB, the impulse first travels down the right bundle branch—the impulse activates the interventricular septum from right to left—the opposite of normal activation. Finally, the impulse activates the left ventricle—the left ventricle fires late

LBBB ECG Features

• Best seen in V1

• QRS complex > or = to .12 seconds

• QRS is predominantly negative in V1

• ST-T wave changes are more prominent than RBBB—often see T wave inversion in Lead I, V5 and V6

LBBB

Myocardial Ischemia & Infarction

Ischemia

Inferior AMI

Reciprocal Changes (Remote Ischemia)

• ST-segment depression in the wall of the heart opposite the location of the infarction

• Inferior MI’s—produce reciprocal changes in the anterior (V1-4) and high lateral (I and aVL)

• Anterior MI’s—produce reciprocal changes in the inferior wall (II, III, aVF)

Reciprocal Changes

Xxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxx

xxxxxxxxxxxxxxxxxxxxxxxxxxxx

Anterior Wall MI

Lateral Wall AMI

Anterior Lateral Wall MI

ECG

Right Ventricular Wall MI

Diagnosing Right Ventricular AMI

When diagnosing a RV AMI—only need ½ mm ST-segment elevation because the muscle of the RV is thin compared to the muscle of the LV which is very thick.

Posterior AMI

• Horizontal ST depression

• Tall, broad R waves

• Upright T waves

• Dominant R wave (R/S ratio > 1) in V2

Electrolyte Imbalances

Hyperkalemia

Serum Potssium (mmol/L) Predicted ECG status 5.5-6.5 Tall tented T waves 6.5-7.5 Loss of P waves 7.5-8.5 Widening QRS 8.5 QRS continues to

widen, approaching to sine wave

Pericarditis

• Widespread ST elevation throughout all leads and without remote ischemia

• PR segment depression

• Q-waves never develop

Pericarditis

• Stage 1 – widespread STE and PR depression with reciprocal changes in aVR (occurs during the first two weeks)

• Stage 2 – normalization of ST changes; generalized T wave flattening (1 to 3 weeks)

• Stage 3– Flattened T waves become inverted (3 to several weeks)

• Stage 4 – ECG returns to normal (several weeks onwards)

Lead II is Helpful

Pulmonary Emboli

ECG

Hypothermia

• Hypothermia is defined as a core body temperature of < 35 degrees centigrade

• Mild hypothermia is 32-35 degrees

• Moderate hypothermia is 29-32 degrees

• Severe hypothermia is < 29 degrees

Hypothermia- ECG Changes

• Bradyarrhythmias

• Osborne Waves (= J waves)

• Prolonged PR, QRS and QT intervals

• Shivering artefact

• Ventricular ectopics

• Cardiac arrest due to VT, VF or asystole

Hypothermia

Left Ventricular Hypertrophy (LVH)

• Compare V1 & V2 and determine which lead has the deepest “S” wave- determine depth mm

• Compare V5 & V6 and determine which leads has the tallest “R” wave- determine in mm

• Add the height of the tallest “R” wave and the deepest “S” wave

• If number is equal to or > than 35 mm, suspect LVH

• Or “R” in aVL is equal to or > 11 mm

Wolffe-Parkinsons-White Syndrome (WPW)

• Syndrome is a congenital abnormality associated with SVT

• There are accessory pathways outside the normal conduction system that bypass the slowing effect of the AV node and rapidly conduct impulses from the atria directly to the ventricles

• Involves activation of the ventricles that occurs earlier than expected (preexcitation)

• Bypasses the AV node- the most common bypass tract is an accessory AV pathway otherwise known as a Kent bundle

WPW

WPW Patients

• Potentially at an increased risk for dangerous ventricular arrhythmias due to extremely fast conduction across the bypass tract

WPW-ECG Finding

• A shortened PR interval (<.12 secs.)- early depolarization of the ventricles

• Delta wave- sloping

• Narrow QRS complex-impulse travels down the AV and travels

up the accessory pathway (more common)

• Wide QRS complex-impulse travels down the accessory pathway and up the AV node

• 25%- normal ECG

WPW- ECG Findings

Practice Time

Brugada Syndrome

• Is a syndrome consisting of syncopal episode(s) and/ or sudden cardiac death in patients with a structurally normal heart

• ECG changes: incomplete RBBB; ST segment elevation in the V1-V3 leads and terminal T wave inversion

• Genetic disposition and predominately affects males

Diagnostic Criteria

• Type 1 (Coved ST segment elevation >2mm in >1 of V1-V3 followed by a negative T wave) is the only ECG abnormality that is potentially diagnostic. This has been referred to as Brugada sign.

Summary

• ECG is the best single test available in the ED

• History is important

• Take your time…don’t jump to the obvious- use a systematic approach