ecg 1 kids
DESCRIPTION
ECG 1 KidsTRANSCRIPT
ECG 1
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
Polarization
• Also called resting membrane potential
• Resting state during which no electrical
activity occurs
• Inside of cell is more negative than outside
Depolarization = Stimulation
• On the ECG:– P wave represents atrial depolarization
– QRS complex represents ventricular depolarization
Depolarization
• Depolarization is not the same as
contraction– Depolarization = Electrical event
• Expected to result in contraction
– Contraction = Mechanical event
• Pulseless electrical activity (PEA)
Repolarization = Recovery
• Return to resting state
• On the ECG:• ST segment represents early ventricular repolarization
• T wave presents ventricular repolarization
Repolarization = Recovery
Properties of Cardiac Cells
• Automaticity
• Excitability
• Conductivity
• Contractility
Action Potential = ALL x NOTHING
Action Potential = opening of sodium and potassium channels
Action Potential
K+ -channels
Na+ -channels
Vm
excitable cell
time
resting potential
Normal Action Potential
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
Cardiac Muscle Action Potential
electrochemicalevents
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
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
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
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!
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
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
Atrial,Ventricular Excitation Timing
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
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
Electrocardiogram• measures the sum
of all electro-chemical activity in the myocardium at any moment– P wave– QRS complex– T wave
Electrocardiogram
Cardiac Cycle• Relationship between electrical and mechanical
events• Systole• Diastole• Isovolumetric contraction• Ventricular ejection• Isovolumetric relaxation
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
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
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
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
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
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”
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?
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
Positive Inotropic Effect• increase the
force of contraction without changing the length of the cardiac muscle cells
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
Regulation of Heart Rate• Intrinsic
– Pacemakers
– Bainbridge effect• Increase in EDV increases HR• Filling the atria stretches the SA node increasing
depolarization and HR
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
Regulation of Heart Rate
Overview
SA NODE
AV NODE
RIGHT BUNDLE BRANCH
LEFT BUNDLE BRANCH
PURKINJEE FIBERS
ELECTRICAL CONDUCTION OF THE HEART
41
Eindhoven’s triangleHeart
Normal Components of the EKG Waveform
P wave• Indicates atrial
depolarization
• Normal duration is not longer than 0.11 seconds (less than 3 small squares)
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
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.
• 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
QRS complex• Represents the spread of the electrical
impulse through the ventricles (ventricular depolarization)
• Normally not longer than .06 - .10 seconds in duration
• 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
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
ST segment
• Indicates early ventricular repolarization
T Wave
• Represents ventricular repolarization
• May be difficult to clearly determine the onset and end of the T wave
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
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.
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?
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
ECG Paper
• ECG paper is graph paper made up of small and larger, heavy-lined squares
– Horizontal axis = Time
– Vertical axis = Voltage/amplitude
6-Second Method
• Count the number of complete QRS complexes within a period of 6 seconds
– Multiply that number by 10
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
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
Sinus Rhythm
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
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
Sinus Arrhythmia
Ventricular Dysrhythmias
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
Ventricular Tachycardia
Torsades de Pointes (TdP)
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
Ventricular Fibrillation (VF)
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
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
Asystole
Pulseless Electrical Activity
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)
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
• 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
SA NODE
AV NODE
RIGHT BUNDLE BRANCH
LEFT BUNDLE BRANCH
PURKINJEE FIBERS
ELECTRICAL CONDUCTION OF THE HEART
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?
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
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