ecg 1 kids

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