NCM 112 Lesson # 2.

Topic: Electrocardiogram Date: 08-27-22

Electrocardiogram (ECG)
 One test but can acquire many data to create plan based on the data gathered in ECG
 Before, ECG in conclusive but it is now used in combination of other tests like
echocardiogram, CT scans, MRI, and other tests

Example of use of Electrocardiogram (ECG):

High amplitude of T waves – indication for hypocalcemia or hypokalemia (more often hypokalemia)
o ICU nurse will immediately draw blood and submit it to the lab to confirm
Hypokalemia – stop potassium chloride drips, decrease potassium in the diet

ELECTROCARDIOGRAM (ECG/EKG)
 a diagnostic tool that measures and records the electrical activity of the heart in exquisite detail.
Interpretation of these details allows diagnosis of a wide range of heart conditions.
 Introduced by Willem Einthoven in 1893 at a meeting of the Dutch Medical Society. In 1924,
Einthoven received the Nobel Prize for his life’s work in developing ECG
 6-lead ECG – bipolar augmented limb leads
o props are on extremities
o Leads I, II, III, aVL, aVR, aVF
 The 12-lead ECG that is used throughout the world was introduced in 1942.
 The 13th and 14th leads
 Developed in 1990s
 Often used in patients with dextrocardia (heart is positioned towards the right instead to the
left)
 In modern ECG, 2 probe used in upper chest (first intercostal space on the left) and mid-axillary
line (where 6 unipolar lead is being placed; purple)

REASONS TO HAVE AND ECG

 Heart problems can produce a wide array of symptoms - without the benefit of an ECG, it may be
impossible to tell whether these symptoms are being caused by a heart problem or just mimics of one.
 Common symptoms that frequently require an ECG include the following:
o Chest pain or discomfort – angina or to rule out heart burn
o Shortness of breath
o Nausea
o Weakness
o Palpitations (rapid or pounding heartbeats or increased awareness of heart beating)
o Anxiety
o Abdominal pain
o Fainting (syncope)

THE HEART
 Systolic blood pressure (LUB)
  Pressure created in the arteries  Diastolic blood pressure (DUB)
(inside the atrium) when the ventricles 
When the ventricles starts to refill,
contract the pressure from the arteries falls
 Ventricle contracts, increase in simultaneously and the atrium
pressure while atrium is filling up contract creating pressure
 Systole  Pressure being filled up when
ventricles fill up with blood
 D
NOTE: conduction will take milliseconds only.
1.
2. Sinoatrial (SA) Node  Will pass the signal to bundle of his
 Initiates electro-conduction of  Signals enter to AV node, valves will
the heart passing it through close
internodal tracts 4. Bundle of His
 Located to the septum that separates
o Vagal stimulation (vagus
the left and right ventricle
nerves instructs the heart to pump)
 Signals enter to bundle of his, septum
 If SA will not start and other parts of will contract
the conduction is the one who initiated
 Signals will be passed to left and right
the conduction, it will not be a normal
bundle branch
rhythm
o Because there is no direct 5. Left and right bundle branch
connection from SA node to AV  Signals enter to L&R bundle branch;
node creating pacing problems lower part of the septum will
 Signals enter to the SA node, atria will contract and some parts of the right
contract and left ventricle (middle part)
 Signals will be passed to Purkinje
3. Atrioventricular Node fibres
 Signals passed from SA node to AV
6. Purkinje fibers
node, will initiate the  Will contract the whole or rest of the
atrioventricular phasing ventricles

PROPERTIES OF CARDIAC MUSCLE

1. Rhythmicity
 ability of the heart to contract at regular timing
  rhythmic activity; one after the other
 each contraction is accompanied by an electrical charge
 an inherent property independent of any stimulation from nerves
 the heart beats with definite rhythm on 4 phases:
a. stimulation
b. transmission
c. contraction
d. relaxation
2. Contractility
 Ability to contract in response to a stimuli
 Ability of the heart to shorten its length or contract in response to stimuli after depolarization
 Intrinsic ability of the heart to change its force of contraction
 Ability of cardiac cells to contract in an organized manner rests in the unique structure of
myocardial cells
3. Automaticity
 Heart is an involuntary muscle
 Ability of the heart to pace or spontaneously initiate or propagate an action potential
(characteristic of pacemaker cell)
 Ability to beat spontaneously and repetitively even without external neurohormonal control
 Not stimulus required to propagate an action potential
4. Excitability/Irritability
 ability of the heart to respond to a stimulus with the strongest possible contraction or none at
all (All or None Law)
 Influenced by: hormonal or nutritional balance, adequacy of oxygen supply, drug therapy and
products of infection

5. Refractoriness
 Ability of the myocardium to prevent from responding to a new stimulus while the heart is still
in a state of contraction in order to preserve cardiac rhythm
 There is time to rest (during conduction: SA node after passing the signal to AV node)
 Stages: Absolute, Relative
6. Extensibility
 Ability of the heart to stretch during diastole as the heart fills with blood
 Starling’s Law of the heart:
o “The longer the fiber length (up to a certain limit), the stronger the contraction.”
 The longer the muscle fiber, the stronger conduction to need to contract
 Stronger voltage is needed to contract the ventricles compared to atria
7. Conductivity
 Ability of the heart muscle fibers to conduct or transmit an electrical impulse to the next cell
(dromotropic characteristic ).
o Ex: SA node to AV node
 For contraction to take place, the heart must conduct impulses via a specialized route.

NOTE: Important properties are rhythmicity, conductivity and refractoriness

12 LEAD ECG
Two main parts:
1. Bipolar Limb Leads
2. Unipolar Limb Leads
PLACEMENT OF LEADS
Limb Leads
 RA: Red right arm (probe on wrist or brachial)
 LA: Yellow left arm
 LL: Green right leg (probe on ankle)
 RL: Black right leg (probe using zero ground to prevent interference in electroconduction); N = no
readings
o “Remeber Your Great Boyfriend”

BIPOLAR STANDARD LIMB LEADS

 Leads I, II, III + Augmented Unipolar Leads: aVR, aVL, aVF
o Ex: Probe augmented on left arm and
left leg, and the reading is on the right
arm
o aVR – OPPOSITE READING
o Lead II – right to left and downward
(lateral reading and superior and
inferior reading); MOST
COMPREHENSIVE READING
o Lead III – superior to inferior
o aVL – probe on the right part, reading
is on the left arm (right to left)
o aVF – augmented on upper
extremities, reading is downward

UNIPOLAR PRECORDIAL LEADS

Chest Leads
 V1 Red 4th ICS RPSB (Intercostal space, Right sternal boarder)
 V2 Yellow 4th ICS LPSB
V3 Green Midway between V2 and V4 (placed after V4; on the 4th rib)
 V4 Brown 5th ICS LMCL (Left mid clavicular line; read the apical area)
 V5 Black LAAL Lateral & horizontal to V4 (Left anterior axillary line)
 V6 Violet LMAL Lateral & horizontal to V4 (left mid axillary line)
 13th and 14th lead – placed if patient has dextrocardia

NOTE:
 “unipolar” because one placement of
leads and reading; Ex: V1 will enter anterior-
posterior (enter the anterior and when reached
the part of the heart to read, will go out to
V1)
 “bipolar” – one point to another point
  V1 – will read the right side of the heart
 V2 – will read the Erb’s point (fifth point of auscultation of the heart)
 V3 and V4 – will read the left ventricle
 V5 and V6 – will read the anterior and posterior of the electrical activity of the heart

ROLE OF THE ECG MACHINE

 The ECG machine is designed to recognize and record any electrical activity within the
heart
 It prints out (as waves) this information on ECG paper made up of small squares 1mm2
TRACING PAPER
5x5 small boxes = 1 large box
Amplitude = upward; how high Duration = horizontal; time of conduction
 1 small box (upward) = 0.1  1 small box (horizontally) = 0.04
millivolt seconds
 10 small box (upward) = 1  5 small boxes/1 big box
millivolt (horizontally) = 0.2 seconds
Ex: high T wave than normal means “peak T  5 big boxes (horizontally) = 1
waves” basing on the amplitude
seconds

 Each electrical stimulus takes the form of a wave and NORMAL Amplitude
so patterns emerge made up of a number of connected
waves. In this way it is possible to calculate the P wave: 0.1-0.2
duration of individual waves (or collection of waves). Q wave: < 0.1
T wave: 0.4-0.5
 10 small squares vertically is equal to
1 millivolt. So it is possible to calculate the
amount of voltage being released within the heart.
If the line is flat at any time in the duration of a
series of waves, it indicates no electrical activity at
that particular moment.
 The direction in which the waves points
indicates whether electricity is moving towards
or away from a particular lead

SINUS RHYTHM
 Name given to the normal rhythm of the heart
where electrical stimuli are initiated in the SA node
and are then conducted through the AV node and
bundle of His, bundle of branches and Purkinje
fibres.
 NSR – normal sinus rhythm
 Depolarization and repolarization of the
atria and ventricles show up as 3 distinct waves
on ECG (QRS Complex). A unique labelling NOTE:
system is used to identify each wave I. 0.6 seconds – completion of one normal conduction
o DEPOLARIZATION – Contract NORMAL VALUE:
o REPOLARIZATION - Relax Duration of normal conduction: 0.56 –
 Less muscle means less cells which means less 0.68 seconds.
voltage

THE WAVEFORMS
Waveform
 movement away from the baseline in either a
positive or negative direction
Segment
 a line in between waveforms
 “isoelectric line”: no conduction happening
 No isoelectric line in QRS
 Can have isoelectric line in ST segment
Interval
 a waveform with a segment
 Ex: PR interval (there is a segment/isoelectric line);
QT interval; ST interval (WOF for myocardial
infarction; elevation or depression)
Complex
 composed of several waveforms
 QRS complex – downward and upward strokes
A. The P wave
 The first wave (p wave) represents atrial depolarization
o Depolarization – give some electricity to contract
 SA node will conduct electrical stimulus to atrium and will
contract. Once atria contracts, p wave will form

B. QRS Complex
 Represents ventricular contraction.
 After the first wave, there follows a short period where the line is flat. This is the point at which the
stimulus is delayed in the bundle of His to allow the atria enough to pump all the blood into the
ventricles.
 As the ventricles fill, the growing pressure causes the valves between the atria and ventricles to close. At
this point, the electrical stimulus passes from the bundle of His into the bundle of branches and Purkinje
fibres. The amount of electrical energy generated is recorded as a complex of 3 waves known
collectively as the QRS complex.
 Measuring the waves vertically shows voltage. More voltage is required to cause ventricular contraction
and therefore the wave is much bigger
C. The Q wave
 Q wave represents depolarization in the septum
 When AV node and bundle of his conduct electricity, septum will contract, forming Q wave
D. The R wave
 R wave represents the ventricular depolarization
 Atrial repolarization embedded – while ventricles are
contracting, atria is relaxing; no distinct wave in ECG
(override)
 From bundle of His to bundle branches then starts in the Purkinje
fibers
E. The S wave
 S wave represents Purkinje fibers depolarization and
relaxation of bundle of His
F. The T wave
 T wave represents ventricular repolarization
 Relax of ventricles, being filled up with blood
 No conduction or decreased conduction
 Diminished – normal in ECG
 High T wave – normal in pregnant women; doubles in amplitude and duration; stomach compress
the heart upward, elevating the heart to the chest wall
G. The ST Segment
 There is a brief period between the end of the QRS complex
and the beginning of the T wave where there is no conduction
and the line is flat.
 A key indicator for both myocardial ischemia and necrosis if it goes up or down
 Two types of ST segments:
1. NSTEMI (Non-ST Elevated Myocardial Infarction)
- associated with M. Infarct happened in posterior part of the heart
- Ex: circumflex artery and right posterior artery (hard to read using ECG thus, appears
depressed ST segment)
o NSTEMI is more related in patients with no elevation of troponin T
 2 Troponins:
1. Trop T
2. Trop I
2. STEMI (ST elevated Myocardial Infarction)
- Common in left anterior descending artery
o Both is associated with heart attack
H. The PR Segment
 Brief period between the end of the P wave and the beginning of the Q wave where the line is flat
(isoelectric line)
 Represents the AV node conduction – travel of signals from SA node to AV node through
internodal tracts
 Prolonged PR segment are indicative of AV block
I. The PR Interval
 Begins with the onset of the P wave and ends with the onset of the QRS complex. This is a physiologic
delay in the AV node

ECG INTERPRETATION (7 step approach)

1. Initial Survey
 Check the presence of waves, position, regularities or irregularities; abnormal patterns or waves
 Normal T wave = 0.4-0.5 small boxes
  High T wave – suspected to have electrolyte problems
 ST elevation – suspected Myocardial Infarct
 Prolonged PR Interval – increased duration on isoelectric line, suspect AV blocks
2. Rhythm Check
 Two types:
1. SINUS RHYTHM – If P wave is present and succeeded by a QRS complex
paced by SA node
2. JUNCTIONAL RHYTHM – if the P wave is absent or the conduction is
initiated by the AV node
3. Rate (Atrial or Ventricular)
3.1 Atrial Rate (P-P)
 Count for small boxes and big boxes and compute atrial rate
3.2 Ventricular Rate (R-R)
 Count for small boxes and big boxes and compute ventricular rate
 It is important to compute for AR and VR because sometimes there are discrepancies in AR and
VR
 REGULAR RHYTHM
o 300 method:
- Count the number of big boxes between P-P for atrial and R-R for ventricular rate
then divide the number to 300
 Use the tip of the P not the base when counting for P-P
 Ex: P-P = 10 big boxes  300/10 = 30 bpm (Atrial Rate) = bradycardic
o 1500 method:
- Count the number of small boxes between P-P for atrial and R-R for
ventricular rate then divide the number for 1500
 1500/30 = 50 bpm
 IRREGULAR RHYTHM
o Count the number of QRS complex in a 6 second strip and multiply it by 10
- 6 second strip = 30 big boxes (normal ECG reading strip)
- Use the lead II to count for QRS complex
- Would be the heart rate in general (not atrial nor ventricular rate)

4. Axis Determination
 Normal axis of conduction:
(+) 90 degrees to (–) 30 degrees
 Axis deviation – heart failure (left or right)
 Leads I and aVF for determination of QRS
 3 methods of QRS axis
1. THUMB METHOD
o faster interpretation of axis
o right thumb = lead I
o left thumb = lead aVF
o deflection of QRS particularly the R
 positive deflection – upward deflection of R
 negative deflection – downward deflection of R
o positive deflection in lead I (right thumbs up); positive deflection in aVF (left thumbs
up)
 2 thumbs up – interpret as normal QRS axis
 o Positive deflection in lead I (R thumbs up); negative deflection of aVF (L thumbs
down)
 1 thumb up (R) only – interpret as right axis deviation meaning the
conduction is going to the R (Right side heart failure)
o Negative deflection in I and positive deflection in aVF
 Interpret as left axis deviation (Left side heart failure)
o Both negative deflection in I and aVF
 Extreme right axis deviation – right ventricular hypertrophy (incompetent
tricuspid valve)

2. PLOT METHOD
o Graph leads I and aVF according to their deflection (positive or negative) on an
inverted X and Y axis graph

3. RECIPROCAL LEAD METHOD

- Check the unipolar and bipolar limb leads (I, II, III, AVR, AVL, AVF) for equiphasic QRS
complex and check its 90-degree angle lead/ reciprocal lead.
o Equiphasic lead – If Q and R have the same amount of boxes/ amplitude from the
isometric line.
o Reciprocals
 AVF to I
 AVL to II
 AVR to III
- Interpretation
o Equiphasic in lead I
 Normal: (+) deflection in AVF
 LAD or ERAD: (-) deflection in AVF
o Equiphasic in lead II
 Normal: (+) deflection in AVL
 RAD: (-) deflection in AVL
 o Equiphasic in lead III
 Normal: (-) deflection of AVR
 ERAD: (+) deflection of AVR

5. Intervals
Note Note Note
PR interval: 0.12-0.2 msec QRS: 0.08 to 0.12 (2–3 small boxes) QT= (M=0.32-0.44) (F=0.32-0.46)

PR INTERVAL
o Greater than in .2 msec indicates AV block
o Less than PR interval seen patient in cardiac overdose especially for CCBs (calcium
channel blockers: amlodipine, nifedipine, etc.)
o 1st degree AV block: if the PR interval is equally (constant) prolonged
 ex: 0.24 secs, 0.24 secs, 0.24 secs
 internodal tracts did not phased
 no signal in internodal tracts thus, AV node phased on its own
 can be seen when there is occlusion (blocked coronary arteries)
 common: left main coronary artery blockage and left anterior descending artery
o 2nd degree AV block/Mobitz type I (Wenckebach): if there are dropped QRS complexes on
an increasing PR prolongation
 Ex: 0.24 secs, 0.28 secs, 0.32 secs
o 2nd degree AV block/Mobitz type II: if there are dropped QRS complexes with equally
prolonged PR interval
 Increasing prolongation then dropped lead/ QRS complex
o 3rd degree AV block (complete heart block): regular R-R intervals, chaotic PR interval, wide
or narrow QRS complex
 Will lead to cardiac arrest (ready the e-cart)
QRS INTERVAL
o More than 3 small boxes = prolongation of QT interval (PROLONGED QT
Syndrome).
 Usually seen at patients taking antihistamines and antiarrhythmic such as Amiodarone
o GONGENITAL PROLONGED QT SYNDROME – Seen in mothers with cardiac
arrest.
QT INTERVAL
o (M=0.32-0.44) (F=0.32-0.46) – females have slightly larger ventricle and repolarization.

6. Final Interpretation
Measurements
ECG INTERPRETATION (Measurements)
Wave Duration Amplitude Axis
P wave 0.1 sec (2-3 small boxes) <2.5 mv 0 to +75 degrees
QRS 0.08 to 0.12 secs Depends on the size +90 to -30 degrees
complex and proximity chamber
QT interval Bazett’s formula:
 Poor man’s guide: 0.4 – 0.44 male or
0.46 in female
 Beyond 0.44 or 0.46, prolongation of QT =
prolonged QT syndrome (pt receiving
anti-arrhythmic and antihistamine)
 Congenital prolonged QT syndrome =
newborn from mother who had cardiac
arrest before pregnancy/delivery
PR interval 0.12 to 0.20 secs = 3-5 small boxes
 Interpret the ECG
o Specify the ff:
- Rhythm (sinus or junctional)
- Rate: AR and VR (tachycardic or bradycardic)
- The site where the dysrhythmia originated
- The mechanism of dysrhythmia
- Ex: junctional rhythm with atrial tachycardia on leads II, III and aVR (written on ECG form)
o If you have normal findings in any of the steps then specify what is normal
EVOLUTION OF ACUTE MYOCARDIAL INFRACTION (MI)
A – still normal
B – ST elevated
C – common in ST elevation in ER
D – after several hours of ST elevation
E – dropped proponent T (NSTEMI); no ST elevation
F – post MI patients; weeks or months after attack; no depression of S
(not classified as elevation, still on the baseline)

ECG ABNORMAL READINGS

Right Bundle Branch Block
 Right sided heart failure
 “R type” – resembles letter R
 Elevate Q

Left Bundle Branch Block

 Left sided heart failure
 “M type” – resembles letter M
 Cardiac drug overdose patients

 Capture beat – cannot classified as

complete beat because QRS too short and
T wave is not on the baseline
 Single ventricular complexes –
resembles the R type; no other types of
waves
 Wide QRS complex

 Asystole – slight wave or flowy wave; rapid

beat sounds; rapid flash of red light on the
monitor in the nurses’ station
 Straight line – does not mean asystole; probe
is removed; constant red light on the monitor

 Atrial flutter usually leads to atrial fibrillation  not

treated immediately  Junctional rhythms
GULO-GULONG HEART
 Left atrial enlargement – because of the
failure to oxygenate the left ventricle, blood deviate to
the left atrium
 Left bundle branch block – hypertrophy of
left ventricle
 Premature ventricular complexes (PVC) – efforts of heart to reset the phasing
 1st degree AV block – patients’ level 1 in ICU unit (ICU nurse care only one level 1 patents for
the whole shift; can have 3-4 level 4)

 Ventricular Tachycardia and Ventricular Fibrillation – two rhythm that can defibrillate or
shockable
 Ventricular tachycardia particularly pulseless
 Ventricular tachycardia with pulse – can see Vtach on the monitor and can feel pulse: manageable
with anti-arrhythmic (Epiphen, Lidocaine, Lidopen)
o DOC: anti-arrhythmic – AMIODARONE (as of 2015 AHA Guidelines)
o Nursing boards DOC anti-arrhythmic – LIDOCAINE

 French word of “turning of the points”

 Combination of Vtachs and Vfibs

THE SIX SECOND ECG

Cardiac Rhythm Simulator
SINUS READINGS

Normal sinus rhythm

 Normal PR interval
 QRS – 2-3 small boxes
 T wave – 3-4 small
boxes (amplitude)
 No ST elevation
Sinus bradycardia
 Normal rhythm but slow phasing
 56 hr – below normal range
 Normal QRS; no ST elevation

Sinus tachycardia
 Normal rhythm but fast phasing
 140 hr – increased heart rate;
above normal range
 Normal amplitude of waves

Sinus arrhythmia
 Normal then short breaks
 Not detrimental; benign
 Usually seen in athletes
(swimmers) – controlled heart
beats and breathing pattern;
sinus bradycardia is normal for
them
 Will go back to normal in time

Sinus exit block

 P wave is present but no QRS

Sinus arrest
 Longer pause (sinus pause)
 SA node did not phase –
totally no conduction
 Intervention: Vagal nerve
stimulation – let the
patient hold the breath and
then bear down (valsalva
maneuver); vagal stimulation (massage the chest and carotid massage)
 If sinus pause did not disappear, give EPINEPHRINE
 ATRIAL READINGS (P)
Premature Atrial Complexes (PAC)
 Problem in signal transmission of SA node
to AV node
 SA node has not yet sent the
signals to AV node but AV
node already started to phase

Atrial Tachycardia
 Heart rate more than 200
 SA node to AV node
phasing is too fast
 Normal phasing of electro
conduction of the heart: 0.4
– 0.44 secs

Atrial fibrillation
 Not enough blood passing to the
ventricles
 Can see edema on hand and
foot
 Usually treated with
cardioversion and pacemakers
 Holter monitor and cardioverter
 Manual cardioverter – do for two hours

Atrial flutter
 Can lead to atrial fibrillation

Wolff-Parkinson-White
Syndrome (WPW)
 Pre-excitation of pathways
 Bundle of Kent – extra
pathway instead of internodal
tract; shortcut from SA to AV
node
 Positive deflection of
QRS
 Not the same as Parkinson’s disease

AV BLOCKS (prolonged PR)

1st AV Block
 Durationof PR INTERVAL
= .12-.2 seconds (3 to 5
small boxes)
 Equally prolonged PR interval

2nd AV Block Type I

 Increasing prolonged PR interval

2nd AV Block Type II

 Increase then dropped (has P
wave but no QRS)
 AV node did not phase after SA
node
 Contract atrium: not contract
ventricle

3rd AV Block

JUNCTIONAL READINGS (no

P)
Premature Junctional
Complex (PJC)
 SA node did not phase; negative deflection
of P but AV node phased

Junctional Rhythm
 Absent P wave

Wandering Pacemaker
 Just like WPW with shortcut
 Intermittent presence of
shortcut
Accelerated Junctional
 Faster junctional rhythm with normal
heart rates

Junctional tachycardia

VENTRICULAR READINGS (QRS)

Premature ventricular complex
 Electro conduction system is off
 SA node and AV node phased at
the same time

Ventricular Tachycardia

Ventricular Fibrillation

Asystole

TREATMENT:
Defibrillation: Ventricular tachycardia (pulseless) and Ventricular Fibrillation
Cardioversion: atrial fibrillation and atrial flutter
Anti-arrhythmic drug: the rest of arrhythmias
 Calcium Channel Blocker (CCB): amlodipen, felodipine, nicardipine; “pine”
 Beta Blocker/Agonists: metoprolol; propranolol; “olol brothers”
  ACE inhibitors: used as adjunct – will synergize the effects of cardiovascular meds or treat
other signs and symptoms of patients like hypertension; “pril sisters”;

ECLS DRUGS
(EXTRACORPOREAL LIFE SUPPORT)
 Amiodarone – DOC for antiarrhythmic drugs; can replace 1st and 2nd dose of
epinephrine
 Lidocaine – can be given after 2 doses of epinephrine

QUESTIONS
ECTOPIA CORDIS
 Individuals with congenital anomalies where
their heart is outside the body
 Limb leads and augmented leads; no
unipolar leads
AMPUTATED INDIVIDUALS/NO
EXTREMITIES
 Use two probes (one on the L 1st intercostal
space, one on midaxillary line/V6)
CARDIOVERSION
 Shock is directed to the anomaly
 Used in atrial flutter and atrial fibrillation
 Example: Just closing one program
 Automatic reading
 If SA node did not phase, pacemaker will
give the phasing
AUTOMATED EXTERNAL
DEFIBRILLATOR (AED)
 Work as defibrillators
 No capacity to act as cardioverters
MANUAL DEFIBRILLATORS
 Has the capacity to act as cardioverters
 Less than 100 joules
 Placed the manual defibrillators on the chest
and midaxillary then deliver the shock to
when there is anomaly

DEFIBRILLATION CARDIAC THUMP

 Shock is delivered anywhere in the ECG  Punching the chest
 Purpose: kill the heart and hoping to  Can deliver more than 360 joules of
revive normally pressure
 Deliver the shock when touching the skin
 More than 360 joules – can
cause
 Example: Just like shutting off the computer
and turning it on again. rupture of the blood vessels or
muscles
PACEMAKER  Not advisable