ECG 1 Kids
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![Page 1: ECG 1 Kids](https://reader034.fdocuments.in/reader034/viewer/2022051318/577cc7ac1a28aba711a1a006/html5/thumbnails/1.jpg)
ECG 1
![Page 2: ECG 1 Kids](https://reader034.fdocuments.in/reader034/viewer/2022051318/577cc7ac1a28aba711a1a006/html5/thumbnails/2.jpg)
Types of Cardiac Cells
• Myocardial cells – Working or mechanical cells
– Contain contractile filaments
• Pacemaker cells – Specialized cells of the electrical conduction system
– Responsible for the spontaneous generation and conduction of electrical impulses
![Page 3: ECG 1 Kids](https://reader034.fdocuments.in/reader034/viewer/2022051318/577cc7ac1a28aba711a1a006/html5/thumbnails/3.jpg)
Polarization
• Also called resting membrane potential
• Resting state during which no electrical
activity occurs
• Inside of cell is more negative than outside
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Depolarization = Stimulation
• On the ECG:– P wave represents atrial depolarization
– QRS complex represents ventricular depolarization
![Page 5: ECG 1 Kids](https://reader034.fdocuments.in/reader034/viewer/2022051318/577cc7ac1a28aba711a1a006/html5/thumbnails/5.jpg)
Depolarization
• Depolarization is not the same as
contraction– Depolarization = Electrical event
• Expected to result in contraction
– Contraction = Mechanical event
• Pulseless electrical activity (PEA)
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Repolarization = Recovery
• Return to resting state
• On the ECG:• ST segment represents early ventricular repolarization
• T wave presents ventricular repolarization
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Repolarization = Recovery
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Properties of Cardiac Cells
• Automaticity
• Excitability
• Conductivity
• Contractility
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Action Potential = ALL x NOTHING
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Action Potential = opening of sodium and potassium channels
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Action Potential
K+ -channels
Na+ -channels
Vm
excitable cell
time
resting potential
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Normal Action Potential
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Cardiac Muscle Action Potential
• Contractile cells near instantaneous
depolarization is necessary for efficient pumping
much longer refractory period ensures no summation or tetany under normal circumstances
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Cardiac Muscle Action Potential
electrochemicalevents
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Cardiac Muscle Action Potentialsarcolemma’s ion permeabilities
opening fast Na+ channels initiates depolarization near instantaneously
opening CA++ channels while closing K+ channels sustains depolarization and contributes to sustaining the refractory period closing Na+ and
Ca++ channels while opening K+ channels restores the resting state
repolarization
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Cardiac Muscle Action Potential
• long absolute refractory period permits forceful contraction followed by adequate time for relaxation and refilling of the chambers
• inhibits summation and tetany
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Pacemaker Potentials• leaky membranes• spontaneously
depolarize• creates
autorhythmicity• the fact that the
membrane is more permeable to K+ and Ca++ ions helps explain why concentration changes in those ions affect rhythm
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Conduction System and Pacemakers
• Autorhythmic cells– cardiac cells repeatedly fire
spontaneous action potentials– Autorhythmic cells: the conduction
system– pacemakers
• SA node – origin of cardiac excitation– fires 60-100/min
• AV node• conduction system
– AV bundle (Bundle of His) – R and L bundle branches– Purkinje fibers
It’s as if the heart had only two motor units: the atria and the ventricles!
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Conduction System and Pacemakers
• Arrhythmias – irregular rhythms: slow (brady-) & fast (tachycardia)– abnormal atrial and ventricular contractions
• Fibrillation – rapid, fluttering, out of phase contractions – no pumping– heart resembles a squirming bag of worms
• Ectopic pacemakers (ectopic focus)– abnormal pacemaker controlling the heart– SA node damage, caffeine, nicotine, electrolyte
imbalances, hypoxia, toxic reactions to drugs, etc.• Heart block
– AV node damage - severity determines outcome– may slow conduction or block it
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Conduction System and Pacemakers
• SA node damage (e.g., from an MI)– AV node can run things (40-50 beats/min)– if the AV node is out, the AV bundle, bundle
branch and conduction fibers fire at 20-40 beats/min
• Artificial pacemakers - can be activity dependent
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Atrial,Ventricular Excitation Timing
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Atrial,Ventricular Excitation Timing
• Sinoatrial node to Atrioventricular node– about 0.05 sec from SA to AV, 0.1 sec to get
through AV node – conduction slows– allows atria time to finish contraction and to
better fill the ventricles– once action potentials reach the AV bundle,
conduction is rapid to rest of ventricles
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Extrinsic Control of Heart Rate
• basic rhythm of the heart is set by the internal pacemaker system
• central control from the medulla is routed via the ANS to the pacemakers and myocardium– sympathetic input -
norepinephrine– parasympathetic input –
acetylcholine
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Electrocardiogram• measures the sum
of all electro-chemical activity in the myocardium at any moment– P wave– QRS complex– T wave
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Electrocardiogram
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Cardiac Cycle• Relationship between electrical and mechanical
events• Systole• Diastole• Isovolumetric contraction• Ventricular ejection• Isovolumetric relaxation
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Cardiac Output• Amount of blood pumped by each ventricle
in 1 minute• Cardiac Output (CO) = Heart Rate x
Stroke Volume– HR = 70 beats/min– SV = 70 ml/beat– CO = 4.9 L/min *
*Average adult total body blood volume = 4-6 L
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Cardiac Reserve• Cardiac Output is variable• Cardiac Reserve = maximal output (CO) –
resting output (CO) • average individuals have a cardiac reserve of
4X or 5X CO• trained athletes may have a cardiac reserve of
7X CO• heart rate does not increase to the same
degree
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Regulation of Stroke Volume• SV = EDV – ESV
– EDV • End Diastolic Volume• Volume of blood in the heart after it fills• 120 ml
– ESV• End Systolic Volume• Volume of blood in the heart after contraction• 50 ml
– Each beat ejects about 60% of the blood in the ventricle
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Regulation of Stroke Volume• Most important factors in regulating SV: preload,
contractility and afterload
• Preload – the degree of stretching of cardiac muscle cells before contraction
• Contractility – increase in contractile strength separate from stretch and EDV
• Afterload – pressure that must be overcome for ventricles to eject blood from heart
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Preload• Muscle mechanics
– Length-Tension relationship?• fiber length determines number of cross bridges• cross bridge number determines force
– increasing/decreasing fiber length increases/decreases force generation
• Cardiac muscle– How is fiber length determined/regulated?– Fiber length is determined by filling of heart – EDV– Factors that effect EDV (anything that effects blood return to
the heart) increases/decreases filling– Increases/decreases SV
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Preload• Preload – Frank-Starling Law of the
Heart– Length tension relationship of heart– Length = EDV– Tension = SV
As the ventricles become overfilled, the heart becomes inefficient and stroke volume declines.
“cardiac reserve”
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Contractility• Increase in contractile strength separate
from stretch and EDV
• Do not change fiber length but increase contraction force?– What determines force?– How can we change this if we don’t change
length?
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Sympathetic Stimulation
• Increases the number of cross bridges by increasing amount of Ca++ inside the cell
• Sympathetic nervous stimulation (NE) opens channels to allow Ca++ to enter the cell
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Positive Inotropic Effect• increase the
force of contraction without changing the length of the cardiac muscle cells
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Afterload• if blood pressure is high, it is difficult for the
heart to eject blood
• more blood remains in the chambers after each beat
• heart has to work harder to eject blood, because of the increase in the length/tension of the cardiac muscle cells
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Regulation of Heart Rate• Intrinsic
– Pacemakers
– Bainbridge effect• Increase in EDV increases HR• Filling the atria stretches the SA node increasing
depolarization and HR
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Regulation of Heart Rate• Extrinsic
– Autonomic Nervous System• Sympathetic - norepinephrine• Parasympathetic – acetyl choline
– hormones – epinephrine, thyroxine– ions (especially K+ and Ca++)– body temperature– age/gender– body mass/blood volume– exercise– stress/illness
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Regulation of Heart Rate
Overview
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SA NODE
AV NODE
RIGHT BUNDLE BRANCH
LEFT BUNDLE BRANCH
PURKINJEE FIBERS
ELECTRICAL CONDUCTION OF THE HEART
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41
Eindhoven’s triangleHeart
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Normal Components of the EKG Waveform
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P wave• Indicates atrial
depolarization
• Normal duration is not longer than 0.11 seconds (less than 3 small squares)
![Page 44: ECG 1 Kids](https://reader034.fdocuments.in/reader034/viewer/2022051318/577cc7ac1a28aba711a1a006/html5/thumbnails/44.jpg)
PR Interval
• PR segment
– Part of the PR interval
– The horizontal line between the end of the P wave and the beginning of the QRS complex
• PR interval = P wave plus PR segment
– Normally measures 0.12 to 0.20 sec
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Only It Doesn’t……• Faster rate• Shorter distances• Resulting intervals are shorter. • PR and QRS intervals gradually lengthen with
age• Key in identifying specific arrhythmias that use
the interval as the criteria for abnormality (e.g., first degree heart block).
• QT interval highly influenced by heart rate. • Faster rate will shorten the interval.
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• PR Interval Based on Age
• Age PR interval• 1 - 3 weeks .07 - .14• 1 - 6 months .07 - .16• 6 - 12 months .08 - .16• 1 - 3 years .09 - .16• 3 - 5 years .09 - .16• 5 - 8 years .09 - .16• 8 - 12 years .09 - .16 • 12 - 16 years .09 - .18
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QRS complex• Represents the spread of the electrical
impulse through the ventricles (ventricular depolarization)
• Normally not longer than .06 - .10 seconds in duration
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• Heart Rate and QRS Interval Based on Age• Age HR QRS interval• 1 - 3 weeks 100 - 180 .03 - .07• 1 - 6 months 100 - 185 .03 - .07• 6 - 12 months 100 - 170 .03 - .08• 1 - 3 years 90 - 150 .03 - .08• 3 - 5 years 70 - 140 .03 - .08• 5 - 8 years 65 - 130 .03 - .08• 8 - 12 years 60 - 110 .03 - .09• 12 - 16 years 60 - 100 .03 - .09
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Developmental Changes in the ECG
Gradual decrease in heart rateGradual lengthening of the PR intervalGradual lengthening of the QRS intervalShift from R to L ventricular dominance
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ST segment
• Indicates early ventricular repolarization
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T Wave
• Represents ventricular repolarization
• May be difficult to clearly determine the onset and end of the T wave
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QT Interval
• Represents total ventricular activity - the time from ventricular depolarization (activation) to repolarization (recovery)
• The duration of the QT interval varies according to age, gender, and heart rate
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QT in Children
• The QT interval based on distance between the initial component of the QRS and the end of the T wave.
• QT interval is highly influenced by heart rate. Faster rate will shorten the interval.
• To adjust for the rate effect on the QT interval, use a "corrected" QT or [Qt.sub.c].
• Qt.sub.c calculated using Bazett's equation of• [Qt.sub.c] = QT interval / square root of RR
interval in seconds.
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Before we start looking at the rhythms
• Why do people have arrhythmias?
• What is the difference between a bad arrhythmia and a not-so-bad arrhythmia?
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What do we look at when reading rhythms
• Assess the rate
• Assess rhythm/regularity
• Identify and examine P waves
• Assess intervals (evaluate conduction)
– PR interval, QRS duration, QT interval
• Evaluate overall appearance of the rhythm
– ST segment elevation/depression
– T wave inversion
• Interpret rhythm and evaluate clinical significance
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ECG Paper
• ECG paper is graph paper made up of small and larger, heavy-lined squares
– Horizontal axis = Time
– Vertical axis = Voltage/amplitude
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6-Second Method
• Count the number of complete QRS complexes within a period of 6 seconds
– Multiply that number by 10
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Rhythm/Regularity
• When analyzing a rhythm strip, determine:– Atrial (P-P intervals) rhythm
– Ventricular (R-R intervals) rhythm
• If rhythm is regular, R-R intervals (or P-P intervals if assessing atrial rhythm) are same
– Plus or minus 10% acceptable
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Sinus RhythmRate 60-100 beats/min
Rhythm Regular
P waves Uniform in appearance, positive (upright) in lead II, one precedes each QRS complex
PR interval
0.12-0.20 second and constant from beat to beat
QRS 0.10 second or less
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Sinus Rhythm
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Sinus BradycardiaRate Less than 60 beats/min
Rhythm Regular
P waves Uniform in appearance, positive (upright) in lead II, one precedes each QRS complex
PR interval 0.12-0.20 second and constant from beat to beat
QRS 0.10 second or less
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Sinus Tachycardia
Rate 101 - 180 beats/min
Rhythm Regular
P waves Uniform in appearance, positive (upright) in lead II, one precedes each QRS complex; at very fast rates it may be difficult to distinguish a P wave from a T wave
PR interval 0.12-0.20 second and constant from beat to beat
QRS 0.10 second or less
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Sinus Arrhythmia
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Ventricular Dysrhythmias
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Ventricular Tachycardia (VT)Rate 101-250 beats/minute
Rhythm Essentially regular
P waves May be present or absent. If present, they have no set relationship to the QRS complexes appearing between the QRS’s at a rate different from that of the VT.
PR interval None
QRS duration Greater than 0.12 second; often difficult to differentiate between the QRS and T wave
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Ventricular Tachycardia
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Torsades de Pointes (TdP)
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Ventricular Fibrillation (VF)
Rate Cannot be determined because there are no discernible waves or complexes to measure
Rhythm Rapid and chaotic with no pattern or regularity
P waves Not discernible
PR Not discernible
QRS Not discernible
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Ventricular Fibrillation (VF)
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Ventricular Fibrillation• This dysrhythmia results in the absence of
cardiac output • The course of treatment for ventricular fibrillation
includes:– immediate defibrillation and ACLS protocols– Identification and treatment of the underlying cause is also needed
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AsystoleRate Ventricular usually not discernible but atrial activity may be
observed (“P-wave” asystole)
Rhythm Ventricular not discernible, atrial may be discernible
P waves Usually not discernible
PRI Not measurable
QRS Absent
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Asystole
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Pulseless Electrical Activity
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PEA – Causes (PATCH-4-MD)
• Pulmonary embolism
• Acidosis
• Tension pneumothorax
• Cardiac tamponade
• Hypovolemia (most common cause)
• Hypoxia
• Heat / cold (hypo-/hyperthermia)
• Hypo-/hyperkalemia (and other electrolytes)
• Myocardial infarction
• Drug overdose / accidents (cyclic antidepressants, calcium channel blockers, beta-blockers, digoxin)
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What do we look at when reading rhythms
• Assess the rate
• Assess rhythm/regularity
• Identify and examine P waves
• Assess intervals (evaluate conduction)
– PR interval, QRS duration,
• Evaluate overall appearance of the rhythm
– ST segment elevation/depression
– T wave inversion
• Interpret rhythm and evaluate clinical significance
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• Every shift print off rhythm strip and place in chart
• Identify – Reg/irreg, PR interval, rate and rhythm– SR, SB, A. Fib, A. flutter, VT and VF – A
MUST– Something is wrong rhythms – the rest
• Know enough to get some help reading them
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SA NODE
AV NODE
RIGHT BUNDLE BRANCH
LEFT BUNDLE BRANCH
PURKINJEE FIBERS
ELECTRICAL CONDUCTION OF THE HEART
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Before we start looking at the rhythms
• Why do people have arrhythmias?
• What is the difference between a bad arrhythmia and a not-so-bad arrhythmia?
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What do we look at when reading rhythms
• Assess the rate
• Assess rhythm/regularity
• Identify and examine P waves
• Assess intervals (evaluate conduction)
– PR interval, QRS duration, QT interval
• Evaluate overall appearance of the rhythm
– ST segment elevation/depression
– T wave inversion
• Interpret rhythm and evaluate clinical significance
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Rhythm/Regularity
• When analyzing a rhythm strip, determine:– Atrial (P-P intervals) rhythm
– Ventricular (R-R intervals) rhythm
• If rhythm is regular, R-R intervals (or P-P intervals if assessing atrial rhythm) are same
– Plus or minus 10% acceptable
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