ECG 1 Kids

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ECG 1

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ECG 1 Kids

Transcript of ECG 1 Kids

Page 1: ECG 1 Kids

ECG 1

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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

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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

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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)

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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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