ECG
 It is a graphical recording of the electrical
activities of the heart.
 It is the first diagnostic test done when
cardiovascular disorder is suspected.
 The procedure is PAINLESS.
INDICATIONS OF ECG
 MI and other CAD
 Cardiac Dysrhythmias
 Heart enlargement
 Electrolytes imbalances- especially CA, NA
and K levels
 Inflammatory diseases of the heart
 Effects of drugs on the heart
ELECTRODE
 An adhesive pad that contains conductive
gel and designed to be attached to the
patients skin
LEADS
 Electrodes connected to the monitor or
EKG machine by wires
 Wires are color coded.
RHYTHM STRIP
 The printed record of the electrical activity
of the heart
The standard ECG consist of 12 leads
 (I, II, III, AVR, AVL, AVF, V1, V2, V3, V4, V5,
V6)
 Used in prehospital and clinics settings
regularly to aid in screening patients who
potential candidates for fibrinolytic therapy
 3 lead ECG- is use to detect life-threatening
dysrhythmias
Bipolar lead/Standard Limb Leads
 Lead I II III - each have one positive
electrode and one negative electrode
 Current flows from the limbs through the
heart
 Lead II and modified chest lead are the
most common leads used for cardiac
monitoring because of their ability to
visualized P waves.
 LA Lead (Black lead) - Should be placed
between the left shoulders and wrist away
from the bony prominences as bone is a
poor conductor of electricity
 RA lead (white lead) should be placed at
the Right shoulder and wrist
 Left Leg Lead (red Lead)-between left leg
and ankle
 Right Leg Lead (Green Lead)- between the
right hip and ankle, sometimes used as an
additional ground lead.
Lead Positive Electrode Negative Electrode
I Left arm Right arm
II Left leg Right arm
III Left leg Left arm
Augmented Leads
 currents flows from the heart outward to
the extremities
 referred to as unipolar lead having one true
pole.
Augmented leads Position of flow
aVR-Augmented Frm the heart to R arm
voltage R arm
aVL-Augmented Frm the heart to L arm
voltage, Left arm
aVF-Augmented From the heart to the L
Voltage-Left foot foot
CHEST LEADS
 from V1-V6
 knows as Unipolar leads or Precordial leads
 Chest leads look at the heart via horizontal
(transverse plane)
 proper placement of the V leads is
important to the correct interpretation of
the 12 lead ECG strip
th
V1- 4 ICS, R sternum
V2-4th ICS, L sternum
V3-5th ICS, halfway between V2 and V3
V4- 5th ICS, Left Midclavicular line
V5- 5th ICS, Left anterior axillary line
V6-5th ICS, Left midaxillary line
V4R- 5th ICS, right midclavicular line
V5R- 5th ICS, right anterior axillary line
It is important that the pts skin be prepared before
attaching the leads. Steps
1. clean the area with an alcohol swab and allow the
area to dry
2. Shave excess hair as indicated
3. If the patient is diaphoretic, attempt to dry the
area or use antiperspirant
4. Use conductive gel to ensure proper conduction
4. Proper placement of the leads
WAVES, COMPLEXES and INTERVAL
P-WAVE
 The first little “hump” or “bump” you see is
known as the P-wave. Remember from the
electrical conduction lecture, that the SA
node is responsible for this.
 Represent The electrical impulse starting
in the SA node spread across atria triggers
atrial contraction
 P wave represents atria depolarization/
contraction (right and left)
 SA node fires first during the a normal
cardiac cycle. This firing send the electrical
impulse outward to stimulate both atria
and manifest as the P wave
 Smooth and upward deflection
 Duration: 0.04-0.11sec
 Normal P wave is 3mm or less
QRS COMPLEX
 a big spike. This spike is called the QRS
complex. The bundle of His, bundle
 branches, and Purkinje fibers are
responsible for this.
 QRS complex represent VENTRICLE
DEPOLARIZATION (contractions of the
ventricles)
 Represents the conduction of the electrical
impulse from the Bundle of His, throughout
the ventricular muscle or ventricular
depolarization/contraction of ventricles
 Duration: 0.05-0.10 sec/ less than 0.12 sec
 Narrow QRS indicates that the impulse is
not form in the ventricles and is thus
supraventricular or above the ventricles
 Wide QRS- the impulse is either ventricular
or supraventricular origin with aberrant
conduction
Q wave
 The first negative deflection or downward
after the P wave
 The first down stroke after the P wave
 3mm in depth
 Normally less than .04 sec I duration
 Pathologic Q wave indicates MI
R wave
 The first positive deflection after the P
wave
 5-10mm in height
 High R waves indicate Ventricular
Hypertrophy- because ehypertrophied
muscles requires a stronger electrical
current to depolarize.
S Wave
 The first negative deflection after the R
wave and terminates at the upstroke of the
T wave
T wave
 Repolarization of the ventricles (the cells
regain a negative charge)
 should exceed 5mm amplitude
 Provides the resting state of the myocardial
work/ Resting phase of cardiac cycle/
 Represents the return of ions to the
appropriate side of the cell membrane
U Wave
- Reperesent repolarization of the Purkinji
fibers
- This wave is rare and it appears in
hypokalemia, HTN and heart disease
- U wave follows the T wave and usually
smaller than the P wave
PR INTERVAL
 As noted on the diagram above, the PR-
interval starts at atrial contraction
(remember atrial contraction is represented
by the P-wave) and ends at the beginning of
ventricle depolarization. So in other words,
it starts at the P-wave and ends at
the beginning of the QRS complex.
 Measure the time interval from the onset of
atrial contraction to the onset of ventricular
contraction
 Represents the Time interval needed for the
impulse to travel from the SA node through
the intermodal pathways in the atria
downward to the ventricles’
 Measured form the onset of P wave to the
onset of the Q wave of the QRS complex.
 Normal PR interval is measured as three to
5 small squares in EKG paper
 Duration: 0.12-0.20 sec
 Shortened PR interval (less than .12sec)
indicates that the impulse was outside the
normal route
 Prolonged PR interval- delay in the
electrical conduction pathway or AV block
J POINT
 It is where the QRS complex meets the ST
segment
 Elevation or depression of 1 mm or more is
an indication of Myocardial injury or
schemia
ST Segment
 Represent early ventricular repolarization,
last from the end of the QRS complex to the
beginning of the T wave
 Represents the plateau phase of the action
potential
 The interval during which the ventricles
are depolarized and ventricular
repolarization begins
ST SEGMENT DEPRESSION
 Due to myocardial ischemia secondary to
myocardial tissue hypoxia
 Hypoxia results in altered repolarization
contribute to ST segment depression
 Characterized by dip below the isoelectric
line of 1-2mm or 1-2 small boxes in the ECG
strip
 Immediate O2 administration
ST segment Elevation
 Due to myocardial injury secondary to
acute myocardial infarction
 Other causes coronary artery spasm,
pericarditis and ventricular aneurysm
QT INTERVAL
- Represents the total time for ventricular
depolarization and repolarization
- Is measured from the beginning of the QRS
complex to the END of T WAVE
- QT interval varies with HR, gender and age.
- Usually 0.32-0.40 secs in duration if the HR
is 65-95bpm
- Prolong QT interval indicated ventricular
dysrhythmia called Torsades De pointes
TP INTERVAL
 - Measured from the end of the T wave to
the beginning of the next P wave-an
isoelectric period
- When no electrical activity is detected the
line on the graph remains flat called
Isoelectric line
- Preferred reference for isoelectric line
PP INTERVAL
- Is measured from the beginning of one P
wave to the beginning of the next P wave.
- Used to determine atrial rate and rhythm
RR INTERVAL
- Is measured from one QRS complex to the
next QRS complex
- Is used to determine ventricular rate and
rhythm.
COMMON ECG changes
Hypokalemia
 U-wave
 Depressed ST segment-
 Short T-Wave
HYPERKALEMIA
 Prolonged QRS complex
 Elevated ST segment- ACUTE MI
 Peak T wave
MI
 Elevated ST segment- acute MI
 Inverted T wave- myocardial ischemia
 Pathologic Q wave
QRS
 Wide QRS- PVC
 Prolonged QRS- Hyperkalemia
Prolonged Q-T interval
 Digitalis toxicity
 Long term quinidine
 Long term procainamide
 hypoglycemia
DETERMINING HR FROM THE ECG
- A 1 minute rhythm strip contains 300 large
boxes and 1500 small boxes.
Accurate method of determining HR and regular
rhythm is to:
- Count the small number of small boxes
within RR interval and divide by 1500 by
that number
- 10 small boxes between two R waves;
- 1500/10= 150bpm
- If there are 25 small boxes
- 1500/25 =60bpm
Inaccurate method of estimating HR, this is used
when the rhythm is irregular
- Count the number of R waves in 6 seconds
x 10
- determining the atrial rate = count PR
interval in 6 seconds multiply by 10
DETERMINING HEART RHYTHM FROM THE ECG
- RR interval is used to determine ventricular
rhythm
- PP interval to determine the atrial rhythm
- If the intervals are the same or if the
difference between the intervals is less than
0.8 secs throughout the strip, the RHYTHM
is regular, if the intervals are different , the
RHYTHM is IRREGULAR.
NORMAL ELECTRICAL CONDUCTION
1.) Impulse starts in the SA NODE (Sinoatrial node)
Study Tip: On exams, you will most likely be asked
what is the “pacemaker” of the electrical system and
the answer is the SA node. The SA node beats at 60-
100 bpm. Furthermore, the SA node represents the
P-wave (atrial contraction) on the EKG tracing.
2.) the electrical impulse travels from the SA node
down through the internodal pathways to the AV
NODE (Atrioventricular node), this process is known
as CONDUCTION.
Study Tip: For exams, know that the AV node is
known as the “gatekeeper“. The AV node is known
for causing a delay of electrical impulse so that the
atrium can fully contract and fills the ventricles with
blood. If there wasn’t a delay the atriums would not
fully empty into the ventricles which would cause
problems. The AV node beats at 40-60 bpm.
3.) Then the impulse travels very quickly through the
BUNDLES OF HIS which branches out into the RIGHT
& LEFT BRANCH BUNDLES
4.) Lastly, the impulse travels to the PURKINJE
FIBERS and then starts all over.
Study Tip: The purkinje fibers beat at 20-40 bpm.
The electrical stimulation is DEPOLARIZATION
causing COTRACTION of Ventricles called SYSTOLE.
Electrical repolarization or relaxation of the
ventricles is called DIASTOLE.
The process from SA node electrical impulse
generation through ventricular repolarization
completes the electromechanical circuit,and the
cycle begins again.
INFLUENCES on HR and CONTRACTILITY
- The heart is influence by ANS which consist
of SNS and PNS
SNS STIMULATION EFFECTS
- increases HR (positive Chronotropy),
conduction through AV node (positive
 dromotropy), and the force of myocardial
contractility (positive inotropy).
- Constrict peripheral blood vessels to
increased BP
- SNS is stimulation is Caused by exercise,
anxiety, fever, administration of
catecholamines, such as dopamine and
dobutamine which increases the incidence
of Dysrhytmias
PNS STIMULATION EFFECTS
- Reduces the HR (negative chronotropy), AV
conduction (negative dromotropy), and the
force of myocardial contraction
- PNS decreases SNS stimulation via rest,
meditation and therapeutic communication
as reduction of anxiety and administration
of beta adrenergic blocking agents may
decrease the incidence of dysrhythmias.
- Decrease Sympathetic stimulation results in
dilation of arteries that lowers BP
- Decreased SNS stimulation (rest, anxiety
reduction methods such as therapeutic
communication, meditation, administering
beta blockers may decreased the incidence
of Dysrhythmias.
NORMAL SINUS RHYTHM
- Electrical conduction that begins in the SA
node generates a sinus rhythm
- NSR occurs when the electrical impulse
starts at regular rate and rhythm in the SA
node and travels through the normal
conduction pathway.
Characteristics
 Ventricular atrial rate: 60-100 bpm in the
adult
 Ventricular and atrial rhythm: Regular
 QRS shape and duration: Usually normal,
but maybe regularly abnormal
 P wave: Normal and consistent in shape;
always in front of the QRS
 PR interval: Consistent interval between
0.12-0.20 seconds
 P:QRS ratio: 1:1
DYSRHYTMIAS
 Disturbances in regular heart rate and
rhythm due to abnormal automaticity,
abnormal conduction or both which affects
cardiac output and blood pressure.
 Are disorders of the formation or
conduction of the electrical impulse within
the heart that alters the HR, rhythm or both
and potentially altered blood flow. A
change of conduction may change the
pumping action of the heart and causes
decrease BP.
 Abnormal cardiac rhythm due to tissue
ischemia, Hypoxemia, SNS and PNS, and
Lactic acidosis, drug toxicity, electrolyte
imbalances
 Dysrhythmias may arise from the SA node
or within the atria or ventricles (known as
ectopy or ectopic beats)
 Dysrhythmias maybe detected by change in
Pulse, or abnormality on auscultation of
heart rate or ECG abnormality.
 Dysrhythmias includes sinus, atrial,
junctional and ventricular and their various
subcategories as well as conduction
abnormalities
 The most common complication in MI is
PVC
 PVC of 6 or more per minute is life
threatening.
SINUS NODE DYSRHYTMIAS
- Originate in the SA node; these includes
sinus bradycardia, sinus tachycardia, and
sinus arrythmia
SINUS BRADYCARDIA
 Occurs when the SA node creates an
impulse at a slower than normal rate
 The heart rate falls below 60 beats/minute
 The parasympathetic fibers are stimulated
and cause the SA node tends to slow.
 The wave of impulse is transmitted through
the normal conduction of pathways.
 Causes: lower metabolic needs (sleep,
hypothyroidism), vagal stimulation
(vomiting, suctioning) medications (calcium
channel blockers (nifedipine, amiodarone),
beta blockers) ICP, and CAD MI, hypoxemia,
delirium.
Signs and Symptoms
- Decrease HR below 60 bpm
- SOB, changes in mental status, chest
discomfort, hypotension
- Locate the PMI or Point of maximum
impulse - 4th or 5th mid clavicular line
Characteristics:
 Ventricular atrial rate: less than 60-100 bpm
in the adult
 Ventricular and atrial rhythm: Regular
 QRS shape and duration: Usually normal,
but maybe regularly abnormal
 P wave: Normal and consistent in shape;
always in front of the QRS
 PR interval: Consistent interval between
0.12-0.20 seconds
 P:QRS ratio: 1:1
 All characteristics of SB are the same as
those of normal sinus rhythm except the
RATE.
 QRS Complex: Normal 2.5 to 3 small boxes
or .10 - .12 seconds

TREATMENT
 Determine the possible cause of the
Dysrhytmia
 If Vagal stimulation such as bearing down
during defecation or vomiting, PREVENT
vagal stimulation
 If beta blockers or calcium channel blockers,
then WITHELD
 Atropine-0.5-1.0 mg IV push blocks vagal
stimulation to the SA node repeated every
3-5 minutes until a maximum of 3mg is
given and therefore accelerates heart rate.
 If unresponsive to atropine, emergency
transcutaneous pacing or catecholamine
such as dopamine and epinephrine is given
 Pacemaker. If bradycardia persist
SINUS TACHYCARDIA
 The SA node creates an impulse at a faster
rate. The heart rate exceeds 100 beats per
minute.
Causes:
 Stress (psychologic or physiologic)- acute
blood loss, hypovolemia, shock, pain,
altered metabolic states (hyperthyroidism),
anxiety, exercise, fever, shock, electrolytes
disturbance(particularly the hyperkalemia)
because the sympathetic fibers are
stimulated speeding up excitation of the
SA node
 Medications that stimulate sympathetic
response (catecholamines, aminophylline,
atropine), stimulants (caffeine, nicotine)
and elicit drugs (cocaine and ecstasy)
 Enhance automaticity of the SA node or
excessive sympathetic tone with reduce
parasympathetic tone
 Autonomic Dysfunction result is a type of
sinus tachycardia known as Postural
Orthostatic Tachycardia Syndrome
characterized by tachycardia without
hypotension when moving to a standing
position with symptoms such as palpitation,
light headedness, weakness, and blurred
vision occurring in standing
 The wave of impulse is transmitted through
the normal conduction pathways; the rate
of sinus stimulation is simply greater than
normal.
Signs
- Increased HR, the diastolic filling time
decreases resulting to decrease CO
- Decreased CO- Syncope, and Low BP
Characteristics
 Ventricular atrial rate: greater than 100
bpm in the adult but usually less than 120
 Ventricular and atrial rhythm: Regular
 QRS shape and duration: Usually normal,
but maybe regularly abnormal
 P wave: Normal and consistent in shape;
always in front of the QRS, buried in the
preceding T wave
 PR interval: Consistent interval between
0.12-0.20 seconds
 P:QRS ratio: 1:1
 All characteristics of Sinus Tachcardia are
the same as those of normal sinus rhythm
except the RATE. ST does not start or end
suddenly.
 If the rapid rate persist and the heart
cannot compensate for the decreased
ventricular filling, it led to Acute Pulmonary
Edema.
TREATMENT
 Synchronized cardioversion is the TOC if
the tachycardia is persistent causing
hemodynamic instability
 Vagal maneuvers by carotid sinus massage,
gagging, bearing down against a closed
glottis (having a bowel movement), forceful
and sustained coughing, or immersing the
face in ice water, it will decrease the HR
 Administer adenocard (adenosine) as this
increased parasympathetic stimulation
causing slower conduction through the AV
node and blocking the reentry of the
rerouted impulse and interrupt tachycardai
 Beta blockers and Calcium channel
blockers- in narrow QRS tachycardia
 Procainamide, amiodarone, and Sotalol in
wide QRS tachycardia
 Digitalis administration (digoxin (Lanoxin)
 Catheter ablation in cases of persistent
inappropriate sinus tachycardia
unresponsive to other treatment
SINUS ARRHYTHMIA
 This occurs when the sinus nodes create an
impulse at an irregular rhythm, the rate
usually increases with inspiration and
decreases with expiration
 Regular irregularity in rhythm which is
related to respiratory exchange
 No treatment is necessary
Characteristics
 Ventricular atrial rate: 60- 100 bpm in the
adult but usually less than 120
 Ventricular and atrial rhythm: irregular
 QRS shape and duration: Usually normal,
but maybe regularly abnormal
 P wave: Normal and consistent in shape;
always in front of the QRS, buried in the
preceding T wave
 PR interval: Consistent interval between
0.12-0.20 seconds
 P:QRS ratio: 1:1
Medical Management
 - No Treatment
SICK SINUS SYNDROME
 A dysrhythmia caused by a disease sinus
node. It is often due to scar-like damage to
electrical pathways in the heart muscle
tissue.
 The sinus node conducts at a slow rate or
fail to conduct at all resulting to sinus block
or pauses
 a group of heart rhythm disorders
These includes:
Sinus bradycardia
 This occurs when the natural pacemaker of
the heart does not send out a signal telling
the heart to beat often enough.
 The heart beat rate is slow.
Supraventricular tachycardia
 This is a fast heart rate that starts in the
upper chambers of the heart (atria).
Tachy-brady syndrome
 This is a pattern of alternating slow and fast
heart rhythms
Sinus pauses or arrest
 This occurs when the natural pacemaker of
the heart stops sending out signals telling
to heart to beat for periods of time.
CAUSES
 It is often due to scar-like damage to
electrical pathways in the heart muscle
tissue.
 Most often occurs in people older than 50.
 In children, heart surgery on the upper
chambers is a common cause of sick sinus
syndrome.
 Tachycardia that start in the upper
chambers of the heart may be part of the
syndrome. These include atrial fibrillation,
atrial flutter, atrial tachycardia, and other
types of fast heart rates. A period of fast
heart rates is often followed by very slow
heart rates immediately after the
tachycardia ends.
Diagnostic Test
 May show abnormal heart rhythms related
to this syndrome.
Holter monitoring
 an effective tool for diagnosing sick sinus
syndrome. It may pick up very slow heart
rates and long pauses, along with episodes
of atrial tachycardias.
TREATMENT
 Treatment of ischemia due to
arteriosclerotic heart disease or MI
 Peace maker
PACE MAKER
 is an electronic device that delivers direct
stimulation to the heart causing to
electrical depolarization and cardiac
contraction
 Initiates and maintains the heart rate when
the natural peacemaker of the heart is not
able to do so.
Permanent implanted pacemaker
 if symptoms are related to bradycardia
(slow heart rate).
ATRIAL DYSRHYTHMIAS
 Originate from foci within the atria and not
the SA node.
 PAC, atrial fibrillation and atrial flutter
PREMATURE ATRIAL CONTRACTION
 also known as atrial premature complexes
(APC) or atrial premature beats (APB).
 this occurs when an electrical impulse
starts in the atrium before the next normal
impulse of the sinus node
 are a common cardiac dysrhythmia
characterized by premature heartbeats
originating in the atria and discharge at a
rate faster than the SA node
 causes: caffeine, alcohol, nicotine, anxiety
hypokalemia, hypermetabolic states, atrial
ischemia, injury or infarction
 PAC is often seen with sinus tachycardia
 The patient might say, My heart skipped a
beat. A pulse deficit may exist (difference
between the apical and radial pulse rate.
Characteristics
 Ventricular atrial rate: depends on the
underlying rhythm
 Ventricular and atrial rhythm: irregular due
to early P WAVES, Short P-Interval, followed
by longer than normal PP interval. This type
of interval in Non compensatory interval
 QRS shape and duration: QRS that follows
the early P waves is usually normal but it
may be abnormal, may be absent (block
PAC)
 P wave: an early and different P wave
maybe seen or hidden in the T wave; other
P wave in the strip are consistent
 PR interval: Early P wave has a shorter than
normal PR interval, but still 0.12-0.20
seconds
 P:QRS ratio: 1:1
Treatment
 does not require treatment if infrequent
 medical management is directed towards
underlying cause (reduction of caffeine
intake, correction of hypokalemia
 Quinidine, Calcium channel blocker, Beta
blockers
  If PAC more than 6 per minute, it indicates
more serious dysrhythmia such as Atrial
Fibrillation
ATRIAL FIBRILATION
 In atrial fib, the electrical flow is chaotic or
there is abnormal impulse formation that
alter the atrial tissue causing the heartbeat
to become irregular, rapid, disorganized
and uncoordinated twitching of the atrial
musculature
 Normally, the heart's electricity flows from
the top chambers (atria) to the bottom
chambers (ventricles), causing the normal
contraction.
 Multiple atrial focci fire impulses at rapid
and disorganized rates
 AFib can be dangerous because it raises
your risk of stroke and heart failure. The
erratic nature of atrial contraction, and
alteration in ventricular ejection and atrial
myocardial dysfunctiom promotes the
formation of thrombi within the left atrium
that increase the risk of embolus resulting
to stroke and heart failure
 Patient with A fib are at risk of heart failure,
ischemia and embolic events such as stroke.
Rapid and irregular ventricular response
reduces the time for ventricular filling
resulting to small stroke volume. Because A
fib causes a loss in AV synchrony (atria and
ventricles contract at different times), atrial
kick or the last part of diastole and
ventricular filling is also lost.
 As a consequence, patients with A fib are
asymptomatic, others may experience
palpitation and signs of heart failure (SOB,
hypotension, Dyspnea on exertion and
fatigue. In addition, High ventricular rate
can lead to mitral valve dysfunction, mitral
regurgitation, intraventricular conduction
delays and dilated ventricular hypertrophy
 May exhibit pulse deficit. The shorter time
in diastole reduces the time available for
coronary artery perfusion increasing the risk
for ischemia or angina
 Atrial may be described as CONTROLLED if
the ventricular response is 100 beats per
minute or less; Uncontrolled if the rate is
above 100 beats per minute
Types Of AFib
Paroxysmal AFib
 A Fib that may come and go
 The episode is momentarily and last for 7
days or lesser and generally go away on
their own
Persistent AFib
 AFib may not go away on their own
 Doctor may perform a procedure or provide
medicine that would bring the heart rhythm
into normal
 Continuous lasting more than 7 days
Long Standing Persistent
- Continuous, lasting more than 12 months
Permanent AFib
 AFib for a long period of time and the heart
may not be able to return the normal sinus
rhythm.
Characteristics
 Ventricular and atrial rate: atrial rate s 300-
600bpm, ventricular rate is 120-200bpm
 Ventricular and atrial rhythm: irregular
 QRS shape and duration: usually normal but
maybe abnormal
 P wave: No discernible P waves. The atria
are not depolarized hence there will be no
well formed P waves. Irregular undulating
waves that vary in amplitude known as
fibrillatory waves
 PR interval: cannot be measured, no P wave
 P:QRS ratio: Many:1
Assessment and Dx
TREATMENT
 Controlled Atrial Fibrillation- no treatment
needed.
 Uncontrolled Atrial Fibrillation- digitalis
preparation to convert it into sinus rhythm
 Class II Beta adrenergic and Class IV Ca
Channel blockers if digitalis and Quinidine is
ineffective to control the heart rate or to
decrease ventricular rate
 Anti thrombotic drugs such as anticoagulant
(heparin and coumadine) and anti-platelet
(aspirin) to prevent stroke
 Anticoagulant for patients with a fib lasting
48 hours or longer to restore sinus rhythm
 Electrical Cardioversion
Electro Cardioversion
- A-fib is hemodynamically unstable
(alteration in mental status, chest
discomfort, hypotension and does not
respond to medications
- Passing an electrical shock of short duration
through the heart to terminate
tachydysrhythmia or to convert
dysrhythmia into normal sinus rhythm.
- Flecainide, propafenone, amiodarone,
dofetilide or sotalol may be given prior to
cardioversion to enhance the success of
cardioversion and maintain sinus rhythm
- Warfarin for at least 4 weeks after the
procedure

CARDIAC RHYTHM THERAPIES
- It includes catheter ablation, maze or mini
maze procedures or convergent procedure
CATHETER ABLATION
- Destroys specific cells that are the cause of
tachydysrhytmia
- Mostly performed for A – fib and recurrent
ventricular tachycardia
- The goal is to eliminate dysrhythmia or
stopping fibrillation
- Similar to cardiac catheterization
- A special catheter is advance near the origin
of the dysrhythmia and high frequency, low
energy sound waves are passed through the
catheter causing thermal injury, localized
cell destruction and scarring. Ablation can
be accomplished using a special catheter to
apply extremely cold temperature to
destroy selected cardiac cells called
cryoablation.
Preoperative Procedure
- Consent
- Shave if necessary
During the Ablation
- Defibrillation pads, an automatic blood
pressure cuff and a pulse oximeter are use
- Moderate sedation is given
- Anesthesia Local in the groin
- IV heparin to reduce the risk of
thromboembolism
- Insertion of the catheter by the AMD
Post Ablation
- Monitor patient for 30 -60 minutes and
retested to ensure dysrhythmia does not
occur. Successful ablation is achieved when
the dysrhythmia cannot be induced
- Monitor LOC closely to ensure recovery
from sedation
- Monitor dysrhythmias, signs and sx of
stroke and vascular access site
complications and fluid imbalances
- Administer pain medications PRN as
ordered.
Risk of Ablation
- AV block, pericardial tamponade, phrenic
nerve injury,stroke, hematoma,pulmonary
vein stenosis, and atrioesophageal fistula
Maze Procedures
 An open heart surgical procedure for
refractory atrial fibrillation
 Small transmural incisions are made
throughout the atria
 Formation of scar tissue prevents reentry
conduction of the aberrant electrical
impulse.
 Some patient may need permanent
pacemaker after the surgery
Mini Maze
- A modification of the maze procedure
- May be performed by making small
incisions between the ribs through which
the video guided instruments are inserted
- Pulmonary veins are encircled with surgical
incisions within the left atrium
- It eliminates the need for opening the
sternum and heart lung by pass
- This results in a shorter recovery time and
lower risk of infection.
Convergent Procedure
- It creates a few small incision in the
abdomen so that a especial catheter can
be inserted through diaphragm toward the
posterior wall of the heart and perform
ablation around the endocardial area of
the pulmonary veins
- Expect mild chest pain due to
inflammation from the ablation.
- Administer pain medications PRN
ATRIAL FLUTTER
 Occurs because of conduction defect in the
atrium and causes a rapid, regular atrial
impulse at a rate between 250-400 bpm.
Very rapid between fairly regular heart
rate.
 Because the atrial rate is faster than the AV
node can conduct, not all atrial impulses are
conducted into the ventricle causing a
therapeutic block at the AV node. Important
feature of this dysrhythmia. If all atrial
impulses were conducted to the ventricle,
the ventricular rate would be 250-400bpm
resulting to ventricular fibrillation
 Occurs with atrial stretching or enlargement
due to MI and CHF
 Conduction of the impulse through the
conduction system is normal and QRS is
unaffected
 A flutter can cause serious signs and
symptoms such as chest pain, SOB, and low
blood pressure
Characteristics
 Ventricular and atrial rate- atrial rate 250-
400bpm, Ventricular rate 75-150bpm
 Ventricular and Atrial Rhythm- Atrial
rhythm is regular and ventricular is usually
regular but may be irregular because of a
change in the AV conduction
  QRS shape and duration: Usually normal,
but may be abnormal or may be absent
 P wave: not present it is replaced by a saw
toothed pattern or F waves that is produced
by rapid firing of the atrial focus
Medical Treatment
 Use of vagal manuevers
Adenosine
 it causes sympathetic block and slowing the
of conduction through the AV node as this
may terminate tachycardia.
 It is given IV by rapid administration and
immediately followed by 20 ml saline flush
and elevation of the arm with the IV line to
promote rapid circulation of the medication
Digitalis and antithrombotic therapy
Beta adrenergic blockers and CA Channel Blockers to
slow AV nodal conduction reverting dysrhytmia
Electrical Cardioversion to convert atrial flutter to
normal sinus rhythm
Paroxysmal Atrial Tachycardia (PAT)
 Sudden onset of an atrial tachycardia with
rates that vary between 140 to 250 beats
per minute
Treatment
Valsalva Maneuver
 this stimulates the vagus nerve to slow the
heart rate
 it is done by having the patient gag or “bear
down” as though attempting to have a
bowel movement
 Perform carotid massage
Adenosine (Adenocard)
 DOC for PAT
Beta Adrenergic Blockers (propranolol)
 Decrease the HR as well as BP
Calcium Channel Blockers (Verapamil)
 Effective in reverting dysrhythmia
Cardioversion/ Counter shock
 Passing an electrical shock of short duration
through the heart to terminate
tachydysrhythmia or to convert
dysrhythmia into normal sinus rhythm.
VENTRICULAR DYSRHYTHMIAS
- originate from the foci within the ventricles
- Premature ventricular complexes,
ventricular tachycardia/ VT, ventricular
fibrillation and idioventricular rhythm
- Ventricular asystole is characterized by
absence of rhythm formation
PREMATURE VENTRICULAR CONTRACTION
 Is an impulse that starts in a ventricle and is
conducted through the ventricle before the
next normal sinus impulse
 An ectopic beat originating in the ventricle
and being discharge at a rate faster than
the next normally occurring beat.
 Can occur in healthy people especially with
intake of caffeine, nicotine and or alcohol
 PVC may be cause by cardiac ischemia, or
infarction, increased workload of the heart
(heart failure), digitalis toxicity, hypoxia,
acidosis or electrolyte imbalances
specifically hypokalemia
 PVC of 6/minute or more is life threatening
it can increase the risk for cardiomyopathy,
and increased the incidence of heart failure.
Etiology
 Acute MI, Electrolyte imbalances,
pulmonary disease, metabolic instability
and drug abuse
Characteristics
 Ventricular and Atrial Rate: maybe low or
fast
 Ventricular and Atrial Rhythm: Irregular due
to early QRS shape and Duration: Duration
is 0.12 or longer. Shape is bizarre and
abnormal
 P wave: Visibility of P wave depends on the
timing of the PVC, may be absent; if the P
wave follows the QRS, the shape of the P
wave is different
 PR interval: not measurable; if the P wave is
in front of the QRS, the PR interval is less
than 0.12 seconds
 P: QRS ratio: 0:1, 1:1
 Patient may feel nothing or may say that
the heart skipped a beat.
Medical Treatment
 Lidocane/IV push/ Drip
Initial Bolus dose: 75-100mg, 50-100mg, 10-15
mg/min
 ProcainamideIV push/ Bolus- 300mg
 Bretyllium- Continuous infusion
 Amiodarone or Sotalol if PVC are frequent
and persistent
LIDOCANE TOXICITY
 Confusion, slurred speech, diminished
mentation, it affects the CNS
VENTRICULAR TACHYCARDIA
 Is define as 3 or 4 more PVC in a row,
occurring at rate of exceeding 100 bpm
 A life threatening that originates from
irritable focus within the ventricle at a rapid
rate.
 It is ineffective rhythm for maintaining CO.
 it is an emergency because the patient is
nearly always UNRESPONSIVE and PULSE
LESS
  Causes: MI and lower ejection fractions are
at higher risk of lethal VT
Characteristics
 Ventricular and Atrial rate: Ventricular rate
100-200bpm or more ; atrial rate depends
on the underlying rhythm
 Rhythm: usually regular but maybe irregular
 QRS and Duration: Duration is 0.12 seconds
or more; abnormal shape, Wide QRS
 P wave: very difficult to detect, absent
 P-R interval: not measurable, very irregular
 P: QRS ration: difficult to determine,but if P
waves are present, there are usually more
QRS complexes than P waves
Treatment
 Antiarrhythmic medication, anti-tachycardia
pacing or direct cardioversion or
defibrillation
Anti-arrhythmic medications
 Procainamide is used for monomorphic
stable VT in patients who do not have acute
MI or severe HF
 Amiodarone IV 300mg/IV push,
then150mg/IV in 3-5 minutes
 Sotalol for stable monomorphic VT
 Lidocaine as Bolus or continuous infusion
Defibrillation- if loss of consciousness occurs, or TOC
for pulseless VT
Cardioversion-if conscious, TOC for monomorphic VT
in symptomatic patient
Sodium bicarbonate- to relieve lactic acidosis
Ventricular Fibrillation
 The ventricles are firing chaotically at rates
that exceed 300 beats per minute and;
Very rapid and uncoordinated heart beats
 do not allow for effective impulse
conduction
 NO CO, NO PULSE, NO BP, LOC
 Most common dysrhythmia in patient with
CA which is rapid, disorganized, ventricular
rhythm that causes ineffective quivering of
the ventricles
 Produces Clinical Death and must be
reverse immediately
 It is an emergency due to absence of heart
beat, pulse and respiration
 Cause: the most common is CAD resulting in
AMI. Other causes unsuccessful V treated
VT acidosis, electrolytes disturbance, and
valvular heart disease
Characteristics
 Ventricular Rate: more than 300 beats per
minute, atrial: No activity
 Ventricular Rhythm: chaotic, extreme
irregular,
 P wave: not present
 QRS: irregular, not recognize
 T wave: not obvious
Medical Treatment
Immediate Defibrillation
 only treatment for VF.
 Use 200-360 joules
 1st defibrillate 200 watts/sec, 2nd defibrillate
200-300 watts/sec; 3rd defibrillate 360
 Pause only to check rhythm and pulse
quickly between these defibrillations
 If the 3rd shock is unsuccessful, begin CPR
and administer epinephrine (adrenaline) 1
mg IV push
 Epinephrine may make the fibrillation more
vulnerable to defibrillation
Na Bicarbonate
 To relieve lactic acidosis
Epinephrine
- 1 mg IV push BOLUS every 3-5 minutes in
cardiac arrest as ordered
Amiodarone
- to facilitate the return of pulse after
defibrillation
IDIOVENTRICULAR RHYTHM
- Aka “ventricular escape rhythm” occurs
when the impulse starts in the conduction
system below the AV node
- When the sinus node fails to create an
impulse or the impulse is created but
cannot be conducted through the AV node
(due to AV block) the Purkinje fibers
automatically discharge an impulse
Characteristics
- Ventricular rate: between 20-40 bpm,
- if the rate exceed 40 bpm, this is
accelerated idioventricular rhythm
- Ventricular rhythm: regular
- QRS shape and duration: Bizarre, abnormal
shape, Duration is 0.12 or more
SS and SX
- LOC and reduce CO
Medical management
- Epinephrine- to increase the HR
- Atropine- to increase HR
- Vasopressor – to increase HR and CO
- Emergency transcutaneous pacing
Temporary emergency pacing
- is indicated for therapy of significant and
hemodynamically unstable
 bradyarhythmias and for prevention of
bradycardia
- temporary cardiac pacing using pads or
paddles applied externally to the chest
INDICATIONS
 hemodynamically unstable bradycardias
that are unresponsive to atropine.
 bradycardia with symptomatic escape
rhythms that don't respond to medication.
 3rd degree heart block
 Mobitz type II second-degree heart block
when haemodynamically unstable or
operation planned
 asystole
METHOD OF INSERTION AND/OR USE
 place pads in AP position (black on anterior
chest, red on posterior chest)
 connect ECG leads
 set pacemaker to demand
 turn pacing rate to > 30bpm above patients
intrinsic rhythm
 set mA to 70
 start pacing and increase mA until pacing
rate captured on monitor
 if pacing rate not captured at a current of
120-130mA -> resite electrodes and repeat
the above.
 once pacing captured, set current at 5-
10mA above threshold
VENTRICULAR ASYSTOLE
- Commonly called flatline, no electrical
activity, no ventricular contraction
- NO HR, NO PULSE, NO RR.
- Characterized by absent QRS complexes
confirmed in two different leads,
- P may be apparent for a short duration
MEDICAL MANAGEMENT
- CPR and identify underlying and
contributing factors
- Intubation and IV access with no or minimal
interruption in chest compressions
- Oxygen
CONDUCTION ABNORMALITIES
- Conduction is altered at the level of the AV
node
Causes
- Medications- digitalis, calcium channel and
beta blockers
- Ischemia and infarction. Cardiomyopathy,
Endocarditis and myocarditis
HEART BLOCKS/AV BLOCKS
 Altered conduction due to impaired tissue
at the level of AV node
 AV block occur when the conduction of the
impulse through the AV node or Bundle of
His area is DECREASED or STOPPED.
 PR interval is assessed for the possibility of
the AV block; prolonged PR interval
TYPES
First Degree AV block
 The impulse is transmitted normally, but it
is delayed longer at the level of the AV node
 P-R interval exceed .20 sec
 Requires no treatment
 ECG Changes- Prolonged P-R interval
greater than .20 secs contantly
Characteristics
 Ventricular and atrial rate: depends on
underlying rhythm
 Ventricular and atrial rhythm: depends on
underlying rhythm
 P-wave and R-waves: Regular
 P-wave always accompanying the QRS
complex, regular in shape
 QRS complex will measure normal
 PR INTERVAL: PROLONGED, greater than
0.20sec
 P:QRS ratio: 1: 1
Second Degree AV Block Type I
 There is repeating pattern in all but one
series of atrial impulses are conducted
through the AV node into the ventricles (4-5
atrial impulses are conducted
 Each atrial impulse takes a longer time for
conduction than the one before, until one
impulse is fully blocked
 the PR interval are progressively
lengthening and then all of a sudden a QRS
complex is missing and then the pattern
starts all over. This is the key in
understanding a Wenckebach.
 This rhythm is CYCLIC and will always
present with progressively lengthen PR
intervals until a QRS complex disappears
and then it will repeat itself.
Characteristics
 P-waves & R-wave will be IRREGULAR
 PR intervals: ABNORMAL, longer with each
succeeding complex until there is a P wave
not followed by QRS. The changes in PR
interval are repeated between each
“dropped” QRS
 QRS complex Missing after P wave
randomly
  P: QRS ratio: 3:2, 4:3, 5:4
Second Degree AV Blocked Type 2
- Only some of the atrial impulses are
conducted through the Av node into the
ventricles
- One being the rhythm is not cyclic, it does
NOT have a pattern.  Second, its QRS
complexes will be IRREGULAR and this is the
opposite for a 3rd degree heart block. Third,
it can have NORMAL PR Intervals, where a
3rd degree heart block does not contain any
PR Intervals.
- The p-waves are nice and regular
while there are some missing QRS
complexes which makes the R-wave
irregular. In addition, there is no
pattern of lengthening p-waves.
Characteristics
- Ventricular and atrial rate: Ventricular rate
is lower than atrial rate
- Ventricular and atrial rhythm: PP interval is
regular (if the patient has normal sinus
rhythm. RR interval is regular but may be
irregular
- P-waves will be regular, however R-wave
are irregular
- PR interval will measure normal (most of
the time)
- NO Pattern
- QRS: Missing QRS Complexes after p-waves
randomly
Third Degree Block
 No impulse from the SA node is transmitted
to AV node into the ventricles
 this is the worst one. It requires major
interventions.
 In this rhythm, the atriums and ventricles
are NOT beating together and are working
independently.
 CO is compromised
Characteristics
 Ventricular and atrial rate: depends on the
escape rhythm and underlying atrial
rhythm; but the ventricular rate is lower
than the atrial rate
 Ventricular and atrial rhythm: PP interval is
regular and RR interval is regular
 P-waves will be Regular AND R-waves will
be Regular
 P-wave will not accompany QRS complexes
and vice versus, hence no relationship
between the atriums and ventricles
 PR interval: Not measurable because the
atriums and ventricles are independent
Treatment- it is directed towards increasing the HR
to maintain normal CO
 First degree block- No Treatment
 Second degree block-
 Atropine Bolus initial TOC
 Transcutaneous pacing/ Ventricular
pacemaker - should be employed in
emergency situation
Assessment
- Possible causes of dysrhythmia- history of
heart disease, COPD
- Medications anti arrhythmic drugs
- Signs of Anxiety
- Signs of decreased CO- syncope (fainting),
dizziness, fatigue, chest discomfort,
palpitation
- Rate and rhythm-apical and peripheral
pulses, note for PD
- Note for extra heart sounds like murmurs,
S3 and S4
- Blood pressures- decline pulse pressures
indicated reduce CO
NURSING DIAGNOSIS
- Decreased cardiac output r/l inadequate
ventricular filling or altered HR
- Anxiety r/l disease process or fear of
unknown
PLANNING
- To eliminate or decrease the occurrence of
dysrhythmia
- To maintain CO
- Reduction of anxiety
NURSING INTERVENTIONS
MONITORING and Managing Dysryhtmia to
maintain CO
- Assess for factors contribute to the
dysrhymia (oxygen deficits, electrolytes
imbalances, caffeine, etc.)
- Monitor BP, PR, rhythm, rate and dept of
RR, and breath sounds to determine
hemodynamic effects
- Obtain 12 lead ECG , continuously monitor
the patient and analyze the strip to track
dysrhythmia
- Monitor ECG changes (Wide QRS, absent P
waves, etc.
- Administer medications as prescribed and
monitor the benefits and SE
- Assist in cardioversion, pacing,
defibrillation
Reducing Anxiety
 - Stay with the patient and provide safety
and security – this assist in reducing
anxiety and foster a trusting relationship
- Encourage verbalization of feelings and
fears, and providing supportive and
emphatic statement

ANTI DYSRHYTHMIC DRUGS

1. FAST SODIUM CHANNEL BLOCKERS 1
 Disopyramide (Norpace)
 Procainamide (Pronestyl)
 Quinidine Sulfate (Cardioquin)
2. FAST SODIUM CHANNEL BLOCKERS 2
 LIDOCAINE (Xylocaine)
 Mexilitine Hcl (Mexitil)
3. FAST SODIUM CHANNEL BLOCKER 3
 TOCAINIDE (TONOCARD)
 PROPANONE (Rythmol)
 FLECAINIDE (Tambocor)
CLASS 2
Beta-adrenergic blockers
 Propranolol (inderal)
 Acebutolol (sectral)
Class 3
 Prolong repolarization
 Adenosine (adenocard)
 Amiodarone (cardarone)
 Bretylium (Bretylol)
Class 4
 Calcium channel blockers
 Verapamil hcl (calan)
 Diltiazem (Cardizem)