introduction to ekg for non-ekg techs

Introduction to EKG for non-EKG Techs

By: Adam Arseneault CCT

Many Slides Courtesy of :Mícheál P. Macken MD MRCPIAnd Roneil Malkani MD

The Run Down

Understanding heart conduction Neurological studies of interest What rhythms to worry about Commonly seen rhythms and conduction

abnormalities Question time

Cardiac Conduction

(Marquette Electronics, 1996 )

Sinoatrial (SA) Node

The Sinoatrial Node is the hearts pacemaker Found in the wall of the right atrium at the

junction with the superior vena cava Rich vagal and parasympathetic innervation Intrinsic range of firing is 60-100 bpm

(French, 2006)

Atrioventricular (AV) Node

Back-up Pacemaker Located in the wall of the right atrium next to the

tricuspid valve Responsible for slowing down conduction from the

atria to the ventricles so atrial contraction can occur This slowing lets the atria slightly overfill the ventricles

to increase cardiac output and the ventricular pump Rich vagal and parasympathetic innervation Intrinsic rate is 40-60 bpm

(French, 2006)

Bundle of His (AKA HIS Bundle)

Starts just at the bottom of the AV Node to where the Left and Right Bundle Branches fork

Located in the right atrium and inter-ventricular septum

It is the route of communication between the atria and ventricles

Intrinsic rate of 40-45 bpm

(French, 2006)

Right and Left Bundle Branches

Left Bundle Branches Conducts to the left ventricle

Right Bundle Branch Conducts to the right ventricle

Intrinsic rate is 40-45 bpm

(French, 2006)

(French, 2006)

Purkinje System

Made up of individual cells just beneath the endocardium

These cells initiate the ventricular depolarization cycle

Located in the ventricles Intrinsic rate 20-40 bpm

Cardiac Conduction

(Marquette Electronics, 1996 )

Conduction in Motion

What is an EKG? Basics: Waveforms are representations of the electrical activity created by

depolarization of the atria and ventricles

With an EKG we can measure the rate and regularity of heartbeats, as well as the size and position of the chambers, the presence of any damage to the heart, and the effects of drugs or devices used to regulate the heart, such as a pacemaker.

What is an EKG? 12-lead ECG

- 10 electrodes required to produce 12-lead ECG.

- – Electrodes on all 4 limbs (RA, LA, RL, LL)

- – Electrodes on precordium (V1–6)

- Monitors 12 leads (V1–6), (I, II, III) and (aVR, aVF, aVL)

- Allows interpretation of specific areas of the heart

- – Inferior (II, III, aVF)

- – Lateral (I, aVL, V5, V6)

- – Anterior (V1–4)

What is an EKG?

What is an EKG?

P Wave (Atrial Depolarization)

QRS Complex (Rapid Ventricular Depolarization)

T Wave (Ventricular Repolarization)

(Wagner, 2006)

Depolarization and Repolarization

Depolarization when a cell membrane's charge becomes positive in order to generate an action potential. Caused by positive sodium and calcium ions going into the cell (concentration gradient)

Repolarization (re-negative) when a cell membrane's charge returns to negative after depolarization. Caused by positive potassium ions moving out of the cell.

What is an EKG?

1mm (small square) = 40 ms

5mm (big square) = 200 ms

Methods for measuring heart rate

For regular rhythms: Rate = 300 / number of large squares in between each consecutive R wave

For very fast rhythms: Rate = 1500 / number of small squares in between each consecutive R wave

For slow or irregular rhythms: Rate = number of complexes on the rhythm strip x 6 (this gives the average rate over a ten-second period)

What is an EKG?

PR Interval QRS Interval QT Interval

Interval Norms

P-Wave

PR Interval Time from beginning of the P wave to the beginning of

the QRS complex (onset of ventricular depolarization) Normal range is from 120 ms – 200 ms

Atrial contraction begins in the middle of the P wave and continues throughout the PR interval

Corresponds to the delay necessary for the ventricles to fill after atrial contraction

The atrial repolarization wave (electrical impulse) is usually hidden by the QRS complex

QRS Complex

Time it takes for the depolarization of the ventricles

Norms – 40 ms to 120 ms measured from the initial deflection of the QRS from the isoelectric line to the end of the QRS complex.

R-wave point when half of the ventricular myocardium has been depolarized

RS line activation of the posteriobasal portion of the ventricles

Ventricular depolarization requires normal function of the right and left bundle branches. A block in either the right or left bundle branch delays depolarization of the ventricles, resulting in widening QRS

Ventricular contraction begins at about half-way through the QRS complex and continues to the end of the T-wave.

Pumping of blood begins when ventricular pressure exceeds aortic pressure, causing the semi lunar valves to open. This is normally at the end of the QRS complex and start of ST segment.

Ventricular Depolarization

(Molson Medical Informatics Project, 2000)

ST Segment

Period from the end of ventricular depolarization to the beginning of ventricular repolarization

Although the ST segment is isoelectric, the ventricles are actually contracting

Elevated or depressed is a hallmark sign of ischemia, CAD or impending MI (STEMI)

Norm 80 ms to 120 ms

(Molson Medical Informatics Project, 2000)

QT Interval Normally 340 ms to 430 ms

Measure from the beginning of the Q wave to the end of the T wave

Represents the total duration of electrical activity of the ventricles

Prolonged QT is associated with an increased risk of ventricular arrhythmias, especially torsades de pointes

QTc is prolonged if > 440ms in men or > 460ms in women

QTc > 500 is associated with increased risk of torsades de pointes

QTc is abnormally short if < 350ms

A useful rule of thumb is that a normal QT is less than half the preceding RR interval

T Wave

Corresponds to the rapid ventricular repolarization Normally rounded and positive Most labile wave in the EKG

U Wave

Thought to represent repolarization of the purkinje fibers

Not always seen Prominent U waves are most often seen in

hypokalemia, but may be present in hypercalcemia, thyrotoxicosis, or exposure to digitalis, or epinephrine

Telemetry Monitoring

Rate per minute Examine R to R regularity Check P waves Measure PR Interval Determine if each P wave is followed by a QRS

complex Examine the QRS Examine the QT Interval

(Wagner, 2006)

Normal Cardiac Rhythm

Rate: 60-100 bpm Regular rate and rhythm PR Interval between 120-200 ms QRS Interval between 40-120 ms QT Interval between 340-430 ms

Sinus Rhythm

Rate: 60-100 bpm Regularity: Regular P-Waves: Regular and 1:1 ratio with QRS PR Interval: PR 120-200 ms

Sinus Bradycardia

Rate: <60 bpm Regularity: Regular P-Waves: Regular and 1:1 ratio with QRS PR Interval: PR 120-200 ms

Sinus Tachycardia

Rate: >100 bpm; usually under 170 bpm Regularity: Regular P-Waves: Regular and 1:1 ratio with QRS PR Interval: PR 120-200 ms

Sinus Arrhythmia

Rate: Any sinus rate Regularity: Irregular P-Waves: Regular and 1:1 ratio with QRS PR Interval: PR 120-200 ms

Nei et al, Epilepsia, 2000

EKG Abnormalities During Partial Seizuresin Refractory Epilepsy

Fifty-one seizures in 43 patients with intractable partial epilepsy

Cardiac rhythm and conduction abnormalities are common during seizures, particularly if they are prolonged or generalized, in intractable epilepsy. These abnormalities may contribute to SUDEP.

21 patients with SUDEP compared with previous study of 43 patients with refractory partial epilepsy – studied ECG changes

Ictal max HR was significantly higher in SUDEP patients than in controls (mean 149 bpm vs 126 bpm)

Ictal cardiac repolarization or rhythm abnormalities 56% in SUDEP vs 39% in controls: not significant

Nei et al, Epilepsia, 2004

EEG and ECG in Sudden Unexplained Death in Epilepsy

Ictal asystole (IA) =preventable cause of sudden unexplained death in Epilepsy

Compared heart rate (HR) characteristics of IA patients to a group of patients with vasovagal (benign, not seizure-related) asystole.

IA was seen in 8 patients, all with temporal lobe epilepsy.

No statistical difference was found in:

– duration of asystole, bradycardia, and baseline HR characteristics

Only significant difference: higher HR acceleration post-asystole in the

controls.

Schuele et al, Epilepsia, 2008

Arrhythmias Encountered in Neurological Conditions (Stroke, Seizures, etc.)

Atrial Bradycardia Supraventricular

tachycardias Atrial flutter Atrial fibrillation

Ventricular

• Ectopic ventricular beats

• Multifocal ventricular tachycardias

• Torsades de pointes

• Ventricular fibrillation

Possible Mechanisms:

Altered parasympathetic/vagal activity Altered sympathetic activity Imbalance between these two arms of the

autonomic nervous system Increased circulating catecolamines

Premature Atrial Contractions

These complexes originate in the atria They often originate from ectopic pacemaker

sites within the atria which results in an abnormal P wave

The complex occurs before the normal beat is expected, and followed by a pause

Premature Atrial Contractions

Rate: Underlying rhythm Regularity: Irregular with PAC's; Compensatory Pause P-Waves: Ectopic P-wave; Differs from Sinus P wave PR Interval: Differs from underlying Sinus P wave

Supraventricular Tachycardia

Regularity: Regular Rate: 140 – 220 bpm P-Waves: Usually blocked by preceding T wave QRS: Generally normal Usually starts and stops suddenly

Atrial Flutter

Rate: Atrial: 240-440 bpm; Ventricular varies

Regularity: Atrial rate regular; Ventricular rate from 2:1 to 8:1

Atrial flutter is characterized by "sawtooth" atrial activity and a conduction ratio to the ventricles of 2:1 to 8:1

Caused by a reentry circuit located in the right atrium Check patients cardiac history, if any

Atrial Fibrillation

Rate: Can vary

Regularity: Irregular

P-Waves: No discernible P-wave present

This is the most common sustained cardiac arrhythmia Characterized by an undulating baseline replacing P

waves and an irregularly irregular ventricular response Check patients cardiac history, if any

Premature Ventricular Contraction A PVC is a depolarization that arises in either ventricle

before the next expected sinus beat altering the normal sequence of depolarization

The two ventricles depolarize sequentially instead of simultaneously

Conduction moves slowly and this results in a widened QRS complex (greater than 120 ms)

Three or more PVC's in a row is considered a run of Ventricular Tachycardia

If it lasts for more than 30 seconds it is designated sustained VT

(French, 2006)

Premature Ventricular Contraction

Rate: Underlying rhythm

Regularity: Irregular

P-Waves: Underlying rhythm

PR Interval: Underlying rhythm

QRS: Severely different from other beats, >120 ms

Ventricular Tachycardia

Rate: >100 bpm to <220 bpm

Regularity: Generally Regular; Can be Irregular

QRS Interval: >120 ms

Treatment: If patient is sleeping – wake them up and see if they are responsive and whether rhythm terminates. Also check whether pt. has AICD

If neither – call Code!

Torsades de Pointes

Torsades de Pointes

Polymorphic ventricular tachycardia (PVT) is a form of ventricular tachycardia in which there are multiple ventricular foci with the resultant QRS complexes varying in amplitude, axis and duration. The most common cause of PVT is myocardial ischaemia.

Torsades de pointes (TdP) is a specific form of polymorphic ventricular tachycardia occurring in the context of QT prolongation; it has a characteristic morphology in which the QRS complexes “twist” around the isoelectric line.

For TdP to be diagnosed, the patient has to have evidence of both PVT and QT prolongation.

Ventricular Fibrillation

Rate: Very Rapid; too unorganized to count Regularity: Irregular; No normal QRS; Waveform varies in

size and shape; No P-waves; No T-waves Treatment is always immediate unsynchronized defibrillation

Ventricular Fibrillation Ventricular Fibrillation is a rhythm in which multiple areas

within the ventricles are erratically depolarizing and repolarizing

There is no organized depolarization, therefore the ventricles do not contract as a unit

The myocardium is quivering - There is no cardiac output This is the most common arrhythmia seen in cardiac arrest

from ischemia or infarction. The rhythm is described as coarse or fine VF. Coarse VF

indicates recent onset of VF. Prolonged delay without defibrillation results in fine VF and eventually asystole

Treatment is always immediate unsynchronized defibrillation

Asystole

No Conduction Asystole represents the total absence of ventricular

electrical activity Since depolarization does not occur, there is no

ventricular contraction This may occur as a primary event in cardiac arrest, or

it may follow VF or pulseless electrical activity (PEA). Treatment: Immediate

Transient Asystole

Asystole can also be transient, a few seconds up to 1 minute or longer, due to vagal hyperactivity

Sleep apnea/Snoring during sleep Valsalva maneuver During seizures : Ictal asystole

Medullary centers in brainstrem Valsalva reflex Other causes

Ancillary Information

• Junctional Rhythms/beats

• AV Blocks

• First, Mobitz I and II, Third degree

• WPW

• Brugada

• Electronic Pacer

Junctional Escape Rhythm

Rate: 40-60 bpm

Regularity: Regular

P-Waves: They will be inverted, and may appear before or after the QRS complex, or they may be absent, hidden by the QRS

PR Interval: If Present PR <120 ms

Premature Junctional Contraction

Rate: Underlying rhythm

Regularity: Irregular

P-Waves: They will be inverted, and may appear before or after the QRS complex, or they may be absent, hidden by the QRS

PR Interval: If Present PR <120 ms

First Degree AV-Block

Regularity: Regular Rate: Underlying rhythm P-Waves: Regular and 1:1 ratio with QRS PR Interval: Constant and prolonged PR

Interval, >0.20 sec

Second Degree AV-Block; Type 1Wenckebach

Regularity: Irregular

Rate: Underlying rhythm

P-Waves: Regular

PR Interval: PR gradually elongates until a dropped beat which leads to a reset

This is usually benign and due to increased vagal activity

Second Degree AV-Block; Mobitz Type 2

Rate: Underlying rhythm

Regularity: Irregular

P-Waves: Regular

PR Interval: P-waves march but not all conducted

This block is bad because it originates below the AV node, the escape rhythm is too slow

Treatment is a pacemaker

Third Degree AV-Block; Complete Heart Block

Rate: Underlying rhythm

P-Waves: Regular but not related to QRS A total lack of conduction through the AV node This conduction defect is dangerous and may progress to

ventricular standstill Treatment is an artificial pacemaker

Wolff-Parkinson-White Syndrome

Short PR interval (< 120ms)

Broad QRS (> 100ms)

A slurred upstroke to the QRS complex (the delta wave)

Pre-excitation refers to early activation of the ventricles due to impulses bypassing the AV node via an accessory pathway

In WPW the accessory pathway is often referred to as the Bundle of Kent, or atrioventricular bypass tract

Can cause tachyarrhythmiaLifeinthefastlane.com

Wolff-Parkinson-White Syndrome

Bundle of KentAccessory Pathway

Brugada Syndrome

Note the pattern resembling a right bundle branch block, the P-R prolongation and the ST elevation in leads V1-V3

Brugada is a recently found arrhythmia that can lead to ventricular fibrillation, also may be inherited.

Brugada.org

Pacemaker Rhythms

If a patient has a pacemaker you may see spikes representing the electrical activity from the pacemaker

You could see a “spike” preceding a wide QRS when ventricular pacing

Or a “spike” preceding P wave when atrial pacing

Ventricular Pacemaker Rhythm

Atrial Pacemaker Rhythm

Atrial and Ventricular Pacing

Left-sided Brain Hemorrhage Causing ST Segment Elevation

Introduction to EKG for non-EKG Techs

By: Adam Arseneault CCT

Many Slides Courtesy of :Mícheál P. Macken MD MRCPIAnd Roneil Malkani MD