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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