BASIC ECG INTERPRETATION 2015. Conduction System Review.
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Transcript of BASIC ECG INTERPRETATION 2015. Conduction System Review.
BASIC ECG INTERPRETATION2015
Conduction System Review
CARDIAC CELLS
Current
Electrical charge flow from one point to another
Voltage
Energy measurement between positive and negative points
Measured in millivolts
CARDIAC CELLS
Action Potential
Five Phase cycle reflecting the difference in concentration of electrolytes (Na+, K+, Ca++, Cl-) which are charged particles across a cell membrane
The imbalance of these charged particles make the cells excitable
Cardiac Cell Action Potential
Phase 0 Depolarization
Rapid Na+ entry into cell
Phase 1 Early depolarization
Ca++ slowly enters cell
Phase 2 Plateau-continuation of
repolarization
Slow entry of Sodium and Calcium into cell
Cardiac Cell Action Potential
Phase 3 Potassium is moved out of
the cell
Phase 4
Return to resting membrane potential
CARDIAC CELLS
Current (flow of energy) of electrolytes from one side of the cell membrane to the other requires energy (ATP) Expressed as volts
Measured as ECG
CARDIAC CELLS
Properties
1. Automaticity
1. Cardiac pacemaker cells create an electrical impulse without being stimulated from another source
2. Excitability
1. Irritability
2. Ability of cardiac muscle to respond to an outside stimulus, Chemical, Mechanical, Electrical
CARDIAC CELLS
3.Conductivity
Ability of cardiac cell to receive an electrical impulse and conduct it to an adjoining cardiac cell
4.Contractility
Ability of myocardial cells to shorten in response to an impulse
CONDUCTION SYSTEM
Sinoatrial Node (SA)
Primary pacemaker
Intrinsic rate 60-100/min
Located in Rt. Atrium
Supplied by sympathetic and para-sympathetic nerve fibers
Blood from RCA-60% of people
CONDUCTION SYSTEM
Atrioventricular Junction
Internodal pathways merge
AV Node
Non-branching portion of the Bundle of His
CONDUCTION SYSTEM
AV Node
Supplied by RCA – 85%-90% of people
Left circumflex artery in rest of people
Delay in conduction due to smaller fibers
CONDUCTION SYSTEM
Bundle of His Located in upper
portion of interventricular septum
Intrinsic rate 40-60/min
Blood from LAD and Posterior Descending
Less vulnerable to ischemia
CONDUCTION SYSTEM
Right & Left Bundle Branches LBB – Left Bundle Branch
Anterior Fasicle
Anterior portion left ventricle
Posterior Fascicle
Posterior portions of left ventricle
Septal Fasicle
Mid-spetum
RBB – Right Bundle Branch Right Ventricle
CONDUCTION SYSTEM
Purkinje Fibers Intrinsic
pacemaker rate 20-40/min
Impulse spreads from endocardium to epicardium
The ECG
ECG
Records electrical voltage of heart cells
Orientation of heart
Conduction disturbances
Electrical effects of medications and electrolytes
Cardiac muscle mass
Ischemia / Infarction
ECG Leads
Tracing of electrical activity between 2 electrodes
Records the Average current flow at any specific time in any specific portion of time
ECG
Types of leads Limb Lead (I, II, III)
Augmented (magnified) Limb Leads (aVR, aVL, aVF)
Chest (Precordial) Leads (V1,V2,V3,V4,V5,V6)
Each lead has Positive electrode
ECG Each lead ‘sees’
heart as determined by 2 factors 1. Dominance of
left ventricle
2. Position of Positive electrode on body
ECG
Lead I
Negative electrode
Right arm
Positive electrode
Left arm
ECG
Lead II
Negative Electrode Right Arm
Positive Electrode
Left Leg
ECG
Lead III
Negative Lead Left Arm
Positive Lead
Left Leg
ECG PAPER Graph Paper
Small boxes
1mm wide; 1 mm high
Horizontal axis
Time in seconds
1 mm box represents 0.04 seconds
ECG paper speed is 25 mm/second
One large box is 5 small boxes and =.20 seconds (.04sec x5)
ECG PAPER
Waveforms
Movement from baseline
Positive (upward)
Negative (downward)
Isoelectric –along baseline
Biphasic - Both upward and downward
ECG
P Wave
First waveform
Impulse begins in SA Node in Right Atrium
Downslope of P wave –is stimulation of left atrium
2.5 mm in height (max)
O.11 sec. duration (max)
Positive in Lead II
A normal ECG waveform
ECG
QRS Complex
Electrical impulse through ventricules
Larger than P wave due to larger muscle mass of ventricles
Follows P wave
Made up of a
Q wave
R wave
S wave
ECG
Q wave
First negative deflection following P wave
Represents depolarization of the interventricular septum activated from left to right
ECG
S wave
Negative waveform following the R wave
Normal duration of QRS
0.06 mm – 0.10 mm
Not all QRS Complexes have a Q, R and S
ECG
T wave
Represents ventricular repolarization
Absolute refractory period present during beginning of T wave
Relative refractory period at peak
Usually 0.5 mm or more in height
Slightly rounded
ECG
U wave Small waveform
Follows T wave
Less than 1.5 mm in amplitude
ECG
J PointPoint where the
QRS complex and ST-segment meet
ECG PR Interval
Measurement where P wave leaves baseline to beginning of QRS complex
0.12 - .20 sec.
QRS Interval
Measurement from beginning of the Q wave until the end of the S wave.
0.06 - .12 sec.
ECG
QT interval
Begins at isoelectric line from end of S wave to the beginning of the T wave - 0.44 sec.
Represents total ventricular activity
Measured from beginning of QRS complex to end of T wave.
ECG Analysis
Determine Rate Normal? Fast? Slow?
Atrial Rate? Ventricular Rate?
Is it Regular? ( R-R and P-P intervals) Regularly irregular ( pattern) or irregularly irregular?
Are P-waves Present? Are there p waves before every QRS?
Is the P-P interval constant?
Is The P-R interval normal?
Is the QRS normal? Is the morphology of the QRS the same?
ECG Analysis Determining Rate
Rate Six Second Method
Two – 3 second markers
Count complexes and multiply x 10
ECG
Normal Sinus Rhythm
Electrical activity activity starts in SA node
AV Junction
Bundle Branches
Ventricles
Depolarization of atria and ventricles
Rate: 60-100 /Regular
PR interval / QRS duration normal
ECG
Sinus Bradycardia Sinus Node fires at a rate slower than
normal
Conduction occurs through atria, AV junction, Bundle Branches and Ventricles
Depolarization of atria and ventricles occurs
In adults – rate is slower than 60 / minute
Rate is regular
Why?
Athletes Vagal Stimulation
Medications Cardiac disease
ECG
Sinus Bradycardia Causes
H’s Hypoxia
Hypovolemia
Hydrogen Ion (acidosis)
Hypo-Hyperkalemia
Hypoglycemia
Hypothermia
T’s Toxins
Tamponade
Tension Pneumothorax
Thrombosis
Trauma
ECG
Sinus Tachycardia SA node fires faster than 100-180/minute
Normal pathway of conduction and depolarization
Regular rate
Why?
Coronary artery disease; Fear; anger; exercise;
Hypoxia;Fever
Treatment:
Treat Cause
Beta-Blockers
ECG
Sinus Arrhythmia The SA node fires Irregularly / Rate 60-
100/min.
Normal pathway of electrical conduction and depolarization
PR and QRS durations are normal
Why?
Respiratory- Increases with inspiration; decreases with expiration
Often in children; Inferior Wall MI; Increased ICP;
Medications: Digoxin; Morphine
ECG
Sinus Arrest SA node fails to initiate electrical impulse
for one or more beats
May see no beats on monitor or other pacemaker cells in the heart may take over
Rate: Variable ; Rhythm: Irregular
Why?
Hypoxia; Coronary artery disease; Hyperkalemia
Beta-Blockers; CA channel blockers; Increased vagal tone
ECG
Premature Atrial Complexes An electrical cell within the atria fires
before the SA node fires
Rate: Usually closer to 100; Irregular rhythm
P wave usually looks abnormal and complex occurs before it should
Why?
Emotional stress; CHF; Acute coronary syndromes
Stimulants; Digitalis Toxicity; etc.
ECG
ECG
ECG
ECG
Supraventricular Tachycardiac (SVT) Fast rhythms generated ‘Above the Ventricles’ Paroxysmal SVT (starts or ends suddenly) Rate – usually 130-250 Why? Stimulants; Infection; Electrolyte
Imbalance
MI; Altered atrial pathway (WPW)-Kent
S & S Lightheadedness; Palpitations; SOB; Anxiety;
Weakness
Dizziness; Chest Discomfort; Shock
ECG
Atrial Flutter Irritable focus within the atrium typically fires at a
rate of about 300 bpm
Waveforms resemble teeth of a saw
AV node cannot conduct faster than about 180 beats/minute
Atrial vs ventricular rate expressed as a ratio
Why: Re-entry- Hypoxia Pulmonary embolism
MI Chronic Lung diseasePneumonia etc.
S & S: SOB; Weakness; Dizziness; Fatigue; Chest discomfort
ECG
Atrial Fibrillation
Irritable sites in atria fire at a rate of 400-600/minute
Muscles of atria quiver rather than contract (fibrillate)
No P waves – only an undulating line
Only a few electrical impulses get through to the ventricles – may be a lot of impulses or a few
A lot of impulses (ventricular rate high- then called atrial fibrillation with rapid ventricular response)
A few impulses (ventricular rate slow – then called atrial fibrillation with slow ventricular response)
ECG AV Block
Delay or interruption in impulse conduction Classified according to degree of block and/or to site of
block
First Degree Block
Impulses from SA node to the ventricles is DELAYED but not blocked
Why? Ischemia
Medications
Hyperkalemia
Inferior MI
Increased Vagal Tone
ECG
ECG
ECG
ECG Second Degree Block Type I - Wenckebach
Lengthening of the PR interval and then QRS wave is dropped
Why? Usually RCA occlusion (90% of
population) Ischemia
Increase in parasympathetic tone
Medications
ECG
ECG
The dropped QRS
ECG
ECG
Second Degree AV Block – Mobitz Type II
Why Ischemia LCA – Anterior MI
Organic heart disease
Important:
Ventricular Rate
QRS duration
How many dropped QRS’s in relation to P waves?
What is the ratio?
ECG
ECG
ECG
Third Degree AV Block (Complete Block)
No P waves are conducted to the ventricles The atrial pacemakers and ventricle pacemakers
are firing independently Why?
Inferior MI
Anterior MI
Serious
ECG
ECG
ECG
ECG Ventricular Rhythms
Are the heart’s least efficient pacemakers Generate impulses at 20-40/min They assume pace-making if:
SA nodes fail, very slow (below 20-40) or are blocked
Ventricles site(s) is irritable
Irritable due to ischemia
Depolarization route is abnormal and longer, therefore QRS looks different and is wider.
T wave is opposite in direction to QRS
ECG Premature Ventricular Contractions
May be from One Site and all look the same
Called Unifocal (from one focus or foci)
ECG May be from Different sites (Foci) and are called
Multifocal PVC’s
ECG May occur every other beat – Ventricular Bigeminy
ECG
May occur every third beat – Ventricular Trigeminy
ECG R on T PVC
ECG
ECG Couplets (2 PVC’s in a row); Triplets (3 PVC’s in a row)
ECG Couplets also known as ‘Salvos’.
ECG Run of PVC’s
Ventricular Tachycardia
ECG Ventricular Tachycardia
Defined as Three or more PVC’s occurring in a row at a rate > 100/min
Wide QRS No P waves No T waves Why?
Ischemia
Infarction
Congenital
Usually lethal
S & S: Weakness, Dizziness, Shock, Chest Pain,Syncope
ECG
ECG
ECG Torsades de Pointes (Twisting of the Points)
Ventricular Tachycardia in which the QRS changes in shape, amplitude and width
Causes: Hypomagnesium
Hypokalemia
Quinidine therapy
S & S: Altered mental status, shock, Chest pain, SOB, Hypotension
ECG
ECG
ECG Ventricular Fibrillation
Chaotic rhythm of the ventricles Lethal if not treated Causes:
AMI
Electrolyte Imbalance
Drug OD’s
Trauma
Heart Failure
Vagal Stimulation
Increased SNS
Electrocutions
Congenitial Heart defects
ECG
ECG
Pulseless Electrical Activity – PEA Rhythm on monitor but no corresponding pulse
Why? Look for Cause!
H’s and T’s
Hypoxia Toxins
Hypovolemia Tamponade, cardiac
Hydrogen Ion (acidosis) Tension Pneumothorax
Hypo-Hyperkalemia Thrombosis (coronary or pulmonary)
Hypoglycemia Trauma (Increased ICP, hypovolemia
Hypothermia
ECG
ECG
Asystole No electrical activity on monitor No pulse Why? Look for Cause! H’s and T’s
Hypoxia Toxins
Hypovolemia Tamponade, cardiac
Hydrogen Ion (acidosis) Tension Pneumothorax
Hypo-Hyperkalemia Thrombosis (coronary or pulmonary)
Hypoglycemia Trauma (Increased ICP, hypovolemia)
Hypothermia
Thanks for Coming!Questions?