Basic Dysrhythmia

Interpretation

NURS 108
Spring 2008
Majuvy L. Sulse RN, MSN,CCRN

Cardiac Cycle

Systole-simultaneous contraction of
ventricles, lasts 0.28 sec
Diastole- ventricular relaxation, lasts 0.52 sec
One cardiac cycle occurs every 0.8 sec

Cardiac Cycle

Stroke volume-volume of blood (70cc)

pumped out of one ventricle of the heart in a
single contraction
Heart rate- number of contractions per
minute(60-100bpm
Cardiac output-amount of blood pumped by
the left ventricle in 1 minute (4-8L/min)

CO= SV XHR

Cardiac Cycle

Preload-degree of myocardial fiber stretch at the end of diastole

Afterload-resistance against which the heart must pump to eject
blood through the semilunar valves and into peripheral vessels
STARLINGS Law-the more the muscle fibers are stretched up to a
certain point, the more forceful the subsequent contraction will be.
Systemic vascular resistance (impedance)- amount of opposition to
blood flow offered by the arterioles, pressure the heart must
overcome to open the aortic valve

Autonomic Nervous System

Sympathetic-prepares for physical activity-fight or

flight response-norepinephrine (Adrenergic nerve
endings)

Alpha-vasoconstriction
Beta

Beta 1-increase HR & contractility

Beta 2-bronchial dilation & vasodilation

Parasympathetic-rest & digest function

Acetylcholine (cholinergic nerve endings)

Electrophysiologic Properties

Automaticity-ability to generate an electrical impulse

spontaneously & repetitively
Excitability-ability to be electrically stimulated or respond
to an electrical stimulus
Conductivity-ability to receive an electrical stimulus and
transmit to other cardiac cells
Contractility-also rhythmicity is the ability to shorten and
cause contraction in response to an electrical stimuluscoordination of contraction to produce a regular
heartbeat

Major electrolytes that affect

Cardiac Function

3 major cations

K-performs a major function in cardiac depolarization and

repolarization
Sodium plays a vital part in myocardial depolarization
Calcium is important in myocardial depolarization and
contraction.

Magnesium-acts as transporter for Na & K across

cellular membranes. Also plays an important function in
muscular contraction

Movement of Ions

Resting cardiac cells (Polarization) inside the cell is

negatively charged. K is greater in the cell; Na greater
outside the cell (positively charged)-Resting membrane
potential
Depolarization (action Potential)-sodium-potassium
exchanged pump resulting in positive polarity inside the
cell membrane. Myocardial contraction occurs.
Repolarization-recovery or resting phase; positive
charges are again on the outside and negative charges
in the inside

Refractory Periods

Ensures that the muscle is totally

relaxed before another action
potential occurs
Atrial muscle-0.15 sec
Ventricular muscle-.25-.30 sec

Refractory Periods
Absolute refractory
period-cardiac muscle
cannot be depolarized.
Corresponds to beginning
of QRS to peak of T wave
Relative refractory periodcardiac muscles
stimulated to contract
prematurely if stimulus is
stronger than normal.
Corresponds with down
slope of T wave

Cardiac Conduction System

Electrical Conduction Pathway

SA node (60-100bpm)
Internodal pathways
AV node ( 40-60bpm)
Bundle of His
Bundle Branches
Purkenje networks (20-40bpm)

EKG

ECG/EKG-a graphic representation of cardiac activity

12 lead-shows electrical activity from 12 different planes of the
heart-used as a diagnostic tool rather than a monitoring device
Electrode-adhesive pad that contains conductive gel and
designed to be attached to skin
Leads-wires generally color coded. For the EKG to receive a
clear picture of electrical impulses, there must be a positive, a
negative and a ground. The exact portion of the heart being
visualized depends on lead placement

EKG Leads

Baseline-isoelectric line-no current flow in the heart;

consists of positive, negative deflections or biphasic
complex
3 or 5 lead- used for monitoring the current cardiac
activity of patients at risk for cardiac abnormalities
Lead ll or MCL1-modified chest leads mostly used
because of ability to visualize P waves. MCL provides a
R sided view of the heart. MCL6-L sided view of the
heart

EKG Leads

Limb leads

Bipolar leads-measures activity between 2

points (I, II, III)
Unipolar leads-positive electrodes onlyaVR, aVL, aVF

Chest leads-6 precordial leads

LIMB LEADS & AUGMENTED LEADS

EKG Graph Paper

Segments and Intervals

Segments and Intervals

P wave-deflection representing atrial depolarization

PR segment-isoelectric line from end of P wave to beginning
of QRS-impulse is traveling through the AV node. PR interval0.12-0.20(time for atrial depolarization-AV node-Purkenje
fibers)
QRS complex-ventricular depolarization. QRS duration of
0.04-.10 sec from QRS to J-point
ST segment-early ventricular repolarization from J-point to
beginning of T wave. Elevations not more than 1 mm or
deflections o.5 mm from isoelectric line
T wave- ventricular repolarization, usually rounded, positive
deflection
U wave-smaller polarity as T wave-slow repolarization- not
normally seen except in hypokalemia
QT interval-total time for ventricular depolarization and
repolarization

HR Determination

6 second method

P-P or R-R interval method

count QRS complexes in a 6 sec strip x 10 (30 large boxes in

6 sec strip)
count number of small blocks in a P- P or R-R interval and
divide into 1500 (no. of small blocks in 1 min)
Count the number of large blocks in an interval and divide into
300 (number of large blocks in 1 minute)

Memory method

ECG Rhythm Analysis

Analyze P waves- P wave is present. shape is consistent,

must be before each QRS
Analyze QRS complex- QRS complex is present &
consistent
Determine atrial rhythm or regularity- check regularity by
assessing P-P or R-R
Determine ventricular rhythm or regularity-check
regularity by assessing R-R
Determine heart rate-use one of the methods
Measure the PR interval-measurement should be
constant and should be between 0.12-0.20
Measure the QRS duration-measurement should be
constant and should be between 0.04-0.10 sec
Interpret the rhythm

General Rules

First & most important, LOOK

at your PATIENT!
Read every strip from left to
right
Apply the systematic approach
Avoid shortcuts and
assumptions.
Ask and answer each question
in the ECG analysis approach

Artifacts

Waveforms outside the heart-interference caused by:

Patient movement wandering baseline
Loose or defective electrodes-lost contact with
patients skin
Improper grounding-in touch with an outside source of
electricity
Faulty EKG apparatus

Normal Sinus Rhythm

SA node generated an impulse that followed a

normal pathway, the heart rate falls within the
range, atrial & ventricular rhythms are regular, P
waves preceded every QRS and QRS is within
0.12sec

Sinus Bradycardia
SA node fires slower than normal
heart rate-less than 60bpm
Rhythm is regular
P wave upright and same shape
PR is constant .12-.20sec
QRS-normal <.12sec

Sinus Bradycardia

Causes:

Adverse effects:

Vagal stimulation, MI, hypoxia

Digitalis toxicity
Medication side effects
Normal to athletes
Dizziness, weakness, syncope, diaphoresis, pallor,
hypotension

Treatment

According to symptoms, atropine to speed up heart rate,

pacemaker

Sinus Tachycardia

SA node fires at a rate faster than normal but

conduction pathway is normal. All criteria for
interpretation are the same except that the heart rate
is faster.

Sinus Tachycardia

Causes
Emotionally upset, pain, fever, thyrotoxicosis, hypoxia,
hypovolemia, inhibition of vagus nerve,
Caffeine, norepinephrine, theophylline
Adverse effects
Angina, dizziness, hypotension, increased in cardiac workload
Treatment
Treat the cause
Medications may be given- betablockers

Sinus Arrhythmia

The only irregular rhythm from the sinus node and has a cyclic
pattern that usually corresponds with breathing
Rate- varies with respiratory pattern
Regularity-irregular in a repetitive pattern
P waves-Upright in most leads, same shape and one to each QRS
P-P interval is irregular
QRS-<.12 sec
Cause-usually caused by breathing pattern but can also heart
disease
Treatment- usually non required

Atrial Dysrhythmias

SA node fails to generate an impulse

Atrial nodes or internodal pathways may initiate an
impulse and follows the conduction pathway
Dysrhythmias of this type are not lethal
Accessory pathway-irregular muscle connection between
atria and ventricles that bypasses the AV node

Premature Atrial Contractions

Causes- atria becomes hyper and fire early caused by

medications, caffeine, tobacco, hypoxia or heart disease
Adverse effects-if frequent can be a sign of impending
heart failure or atrial tachycardia or fibrillation
Treatment-O2, omit caffeine, tobacco or other
stimulants. Give digitalis or quinidine, treat heart failure.

Premature Atrial Contractions

Rate

normal

Rhythm

usually regular except for a PAC

P waves
shaped differently from a
normal P
wave or
hidden in preceding T wave
PR interval

.12 to .20sec

QRS

.12sec similar to underlying rhythm

Supraventricular Tachycardia
(SVT)

Tachycardia (>150 bpm) originating above the ventricles-SA

node, atria, AV nodes
P waves not discernible-hidden in T waves
Paroxysmal-starts & ends abruptly
Causes-same as PAcs
Adverse effects- palpitations, light-headedness, dizziness,
shortness of breath, chest pain, fainting =decreased cardiac
output
Treatment-vagal maneuvers (cough, bear down), carotid
massage, or medications digitalis, calcium channel blockers,
beta blockers, Adenosine

Supraventricular Tachycardia
(SVT)

Rate

150-250bpm

Rhythm

regular

P waves

not discernible

PR

not discernible

QRS

usually less than .10sec

Atrial Flutter

Results when one irritable atrial foci fires out regular impulses at a
rapid rate that P waves are in a sawtooth pattern
Av node (gatekeepers) cannot depolarize fast enough to keep up,
many impulses never get through to ventricles. Conduction ratio is
variable-2:1block, 3:1 block or 4:1 block. Slow ventricular responseVR of <60pm; rapid VR >100-150bpm)
Causes-acute MI, CHF, digitalis toxicity, pulmonary embolism, SA
node disease, septal defects
Adverse effects-decreased cardiac output
Treatment-digitalis, cardioversion, calcium channel blockers,
ablation

Atrial Flutter

Rate

atrial 250-300bpm, ventricles-variable

Rhythm
regular if conduction ratio is constant,
irregular if conduction rate varies
P waves

replaced by fluttery waves

PRnot measurable
QRS

<.12sec

Atrial Fibrillation

Most common atrial dysrhythmia in elderly patients

Multiple atrial impulses from different locations all at the same time
(350-600bpm)
Ventricular response maybe rapid (100-150bpm) or slow (< 60bpm)

Causes-maybe chronic MI CHF, valvular heart disease,

hyperthyroidism
Adverse effects-decreased cardiac output, blood clots which
can cause MI, stroke or clot in the lung
Treatment- Digitalis, quinidine, cardizem, anticoagulant as
coumadin, cardioversion

Atrial
Fibrillation

Junctional Rhythms

Arrhythmia originating in AV node

HR= 40-60bpm; accelerated =60-100bpm; junctional= 100-140bpm
P wave-absent, inverted before or after a QRS
PR interval-<.12if P precedes a QRS
QRS <.12sec
Cause-vagal stimulation, hypoxia, ischemia of SA node, MI, digitalis
toxicity
Treatment-varies according to type of arrhythmia. Atropine to
increase HR, withhold or decrease medication that can slow heart
rate

Junctional Rhythms

Ventricular Dysrhythmias

Ventricles serves as pacemaker

Heart rate significantly reduced (20-40 beats per
min
Normal conduction system bypassed
QRS bizarre in appearance & >0.12 sec
P waves absent (buried or hidden in QRS)
Rhythms considered life threatening

Premature Ventricular
Complexes (PVCs)

A single ectopic (out of place) complex from an irritable site

Indicates increased myocardial irritability
Precursors of more serious lethal rhythms
Cardiac output compromised
Causes

Myocardial ischemia, Emotional stress, increased physical exertion,

CHF, electrolyte imbalance, digitalis toxicity or acid base imbalances

Treatment- based on symptoms and causative factors

O2 and antidysrhythmics

PVCs

Unifocal-arise from one single site

Multifocal- originate from different sites
Ventricular bigeminy- every other beat is a PVC
Ventricular trigeminy-every third beat is a PVC
Ventricular quadrigeminy- every 4th beat is a PVC
Interpolated- a PVC between two sinus beats
Couplet or repititive PVCs- two PVCs occurring together
without a normal complex in between
Salvos-3 or more PVCs in a row (Vtach)

Premature Ventricular
Contraction (PVC)

Unifocal PVCs

Multifocal PVCs

Premature Ventricular
Contraction (PVC

Bigeminy

NSR with Couplets

Ventricular Tachycardia

3 or more PVCs in a row overriding pacemaker

Sustained-lasts more than 30 sec
Unsustained- less than 30 sec
Can be tolerated for short bursts but can cause profound shock if
unconscious or untreated
Causes- as with PVCs
Treatment
Pulseless Vtach-treated like Vfib
Stable-drug intervention
Lidocaine, procainamide, amiodarone
Unstable- defibrillation

Ventricular Tachycardia

Rate

100-25bpm

Regularity usually regular

P waves

none

PR will vary if present

QRS

wide & bizarre >0.12

Ventricular Fibrillation
(VFib)

Fatal, most common initial rhythm in cardiac arrest

Myocardial cells quiver rather than depolarized
Usually coarse (amplitude > 3mm) then becomes fine (amplitude
less than 3mm)
No cardiac output- cardiovascular collapse
Causes- MI, drug toxicity or overdose, hypoxia, CAD
Treatment- immediate defibrillation must be done, CPR, epinephrine
(medications make defibrillations more successful and prevent
recurrence

Ventricular Fibrillation
(VFib)

Rate

cannot be counted

Regularity

rapid, not detectable

P waves

none

QRS

none detectable

Asystole

Cardiac standstill
Absence of all ventricular activity-no waveforms
Check on 2 leads-? Very fine Vfib
Clinical death-absence of pulse and respirations
Causes- MI, cardiac trauma, ventricular aneurysm,
CHB
Treatment-atropine to reverse vagal influences,
epinephrine, CPR, pacemaker, dopamine, O2

Ventricular Asystole

Rate

zero

Regularity

none

P waves

none

QRS

none

Atrioventricular Blocks

Impulses in the SA node are blocked or delayed-heart blocks- (PR

>.20, some Ps not followed by QRS; some P-P with regular interval
Underlying rhythm is sinus
Rate normal or slow-symptomatic or asymptomatic
Site of block is either AV node or bundle branches
First dgree
Second degree
Type l-Mobitz l
Type ll- Mobitz 2
Third degree

First degree AV block

Prolonged PR interval that results from a delay in the AV

nodes conduction of sinus impulse to ventricles
All parameters are normal except for prolonged PR
interval (hallmark of 1st degree)
Usually asymptomatic
Causes-AV node ischemia, digitalis toxicity, use of
betablockers or calcium blockers
Treatment- treat cause

First Degree AV Block

Rate

based on underlying rhythm

Regularity

usually regular

P waves

upright, one to each QRS

PR interval

> .20 sec

QRS

<.0.12 sec looks alike

Second Degree Block

(Mobitz l (Wenckebach

Progressive prolongation of the impulse

Cyclic pattern is produced: PR interval continues to
increase in length until an impulse is not conducted
(QRS dropped)
Atrial rhythm is regular but ventricles ar irregular
Cause-MI, digitalis toxicity, n\medication effects
Treatment-atropine if heart rate is slow &
asymptomatic, pacemaker.

Second Degree Block

(Mobitz l (Wenckebach)

Rate-Atrial rate normal: ventricular rate less than atria

Regularity-maybe regular or irregular
P waves-normal P; PR interval progressive
prolongation
QRS=<0.12 if at AV node > if block is at bundle branch

Second Degree Block-Mobitz

ll

Increased risk of progression to 3rd degree

Ratio of P waves to QRS complexes (2:1 block, 3:1 block
or 4:1 block)
PR interval is constant or regular for every conducted
beat
Intermittent absence of QRS
Causes-same as type l
Treatment-02, atropine if patient is symptomatic,
epinephrine, dopamine, pacemaker if block continues
and symptoms are present

Second Degree Block-Mobitz

ll

Rate =atrial 60100: ventricular

half of atrial rate
Regularity=regular
P waves= Normal
PR interval=
constant
QRS= <.12 sec or
>.12 sec if BBB
present

Third Degree or Complete

Heart Block (CHB)

SA node sends out impulses as usual but not one is conducted

to the ventricles
Atria & ventricles beat independently of each other-AV
dissociation
Rate- atria-60-100, Ventricles-20-60
Regularity-Regular
P waves- no relationship with QRS
PR interval- no pattern, varies
QRS-based on site of pacemaker
Cause-MI, lesion on conduction system, hypoxia, medication
side effects
Treatment-pacemaker insertion

Third Degree or Complete

Heart Block (CHB)

PACEMAKERS

PACEMAKERS

Device that substitutes for the normal pacemaker of the hearts

electrical conduction system

Generator-controls rate & strength of each electrical impulse

Lead wires-electrode at the tip relay the electrical impulse from the
generator to the myocardium

Types

Temporary-used to sustain HR in an emergency situation

Transcutaneous (TCP)-external cardiac pacing

Transvenous-lead wire threaded through the skin into a large vein

Permanent- implanted in patients chest

Indications for insertion of

Pacemakers

Temporary

Suppression of ectopic atrial or ventricular rhythm

Acute MI with symptomatic bradycardia, 2nd & 3rd degree AV
block or bundle branch block
Maintenance of adequate HR during special procedures or as
prophylaxis after an open heart surgery
Termination of AV nodal reentry

Permanent

Chronic atrial fibrillation with slow ventricular response

Fibrotic or sclerotic changes in the cardiac conduction system
Sick sinus syndrome or Sinus node dysfunction
Tachyarrhythmias
Symptomatic bradycardia and Third degree AV block not

responding to pharmacologic interventions

Permanent Pacemakers

Atrial- lead wire inserted into the Right atrium-stimulates the

atrium then travels down the electrical conduction through the
ventricles

Permanent Pacemakers

Ventricular- lead wire inserted into the Right ventricle.

The electrical impulse from the pacemaker generator
produces ventricular depolarization

Permanent Pacemakers

AV sequential- two electrodes on the lead wire one

placed on the R atrium & one on the R ventricle. Artificial
impulses stimulate or pace first the atria, then the
ventricles

Rules for interpretation of

Pacemaker Rhythms

Same as for dysrhythmias

Remember: Properly functioning
pacemakers will produce rhythms with
pacemaker spikes. Spikes indicates only that
the pacemaker is firing. They do not reveal
information relative to ventricular contraction.
Assess your patient for presence of
symptoms

Code System

1st letter-chamber being paced

A-atrium
V-ventricle
D-dual (both)
2nd letter- chamber sensed
A-atrium
V-ventricle
D-dual (both
O-off
3rd letter- type of response by pacemaker to sensory
I-Inhibited (pacemaker will not function when the
persons heart beats
O-none
T-triggered
D-dual

Code System

4th letter- ability of generator to be programmed

O-none
P-Simple programmability
M-Multi programmability
C-Telemetry ability
P-ability of rate to change with activity

5th letter-ability of generator to defibrillate

P-Antitachycardia
S-Shock
D-antitachycardia processing & shock
O-none

Common Problems
associated with Pacemakers

Battery failure

Decreased amplitude of pacemaker spike and a slowing

pacemaker rate
Immediate transport to the hospital depending on the
patients symptoms or underlying rhythm

Runaway Pacemakers

Rapid rate of electrical impulse discharge results

Immediate transport to a hospital

Failure to Sense

Failure to sense -pacemaker fails to sense the

patient's own intrinsic rhythm and generates a pacer
spike in the intrinsic rhythm's own QRS, absolute or
relative refractory period of the T wave. The
ventricular capture following the pacer spike may or
may not occur. This can cause lethal arrhythmia.
Failure to sense can be caused when the sensitivity
setting is too low.

Failure to Sense

EKG Characteristics: Rate: It may be regular or

irregular. Rhythm: It can be any intrinsic rhythm in
which the pacemaker spike is in the QRS, absolute,
or relative refractory period of the T wave. QRS
complex: It is within the normal limits of the intrinsic
rhythm.
Nursing Intervention: Obtain the blood pressure,
pulse, respiratory rate, O2 saturation and notify the
MD. Closely observe for ventricular tachycardia
caused by failure to sense.

Failure to Capture

Failure to capture of a pacemaker happens

when the output is too low, resulting in a
failure to depolarize the ventricle, which
causes an absence of a mechanical
contraction of the ventricle, or no QRS. It
can occasionally happen or be constantly
happening which results in ventricular
standstill and a pulse-less patient.
EKG Characteristics: Rate: It will be
irregular due to the failure to produce QRS.
Rhythm: The pacemaker spike or spikes will
not have a QRS following them. P Wave: It
may be absent or present. QRS Complex: A
loss of a QRS behind a pacer spike.

Failure to Capture

Nursing Intervention: Should the loss to capture be

occasional, one should get a blood pressure, pulse
rate, respiration rate, and O2 saturation. This is to
determine if the patient is tolerating the failure to
capture. If the failure to capture is continuous, the
patient will be pulse-less or have a symptomatic
bradycardia. This can range from a situation in
which medication may be needed, or a code
situation in which one would follow hospital
protocol. External pacing may be an option for this
patient

Pre-procedure & Post

procedure care

Consent
VS
Skin prep
Pre-op checklist-NPO, dentures, pins
Position post op is important
Maintain hemodynamic stability
Prevent complications

Patient & family Teaching

Guides

Follow the instructions for pacemaker site skin

care. Report any fever or redness, swelling, or
drainage from incision site.
Keep your pacemaker identification card in
your wallet and wear a medical alert bracelet
Take your pulse for 1 full minute at the same
time each day and record the rate in your
pacemaker diary. Take your pulse anytime you
feel symptoms of a possible pacemaker
failure and report them to your physician.

Patient & family Teaching

Guides

Know the rate at which your pacemaker is set and the basic
functioning of your pacemaker, battery failure. Know what
changes to report to your physician.
Report any of the following symptoms to your physician:
dizziness, difficulty of breathing, fainting, chest pain, weight
gain, and prolong hiccupping. If you have any of these
symptoms, check your pulse and call your physician.
Take all medications, follow prescribed diet, activity
restrictions
Do not apply pressure over the generator. Avoid tight clothing
or belts.

Patient & family Teaching

Guides

Do not operate electrical appliances over pacemaker as

they may cause malfunction.
Be sure electrical appliances or motors are properly
grounded.
Avoid all transmitter towers for radio, TV and radar.
Radios, TV, & other home appliance and antennas do
not pose a hazard.
Inform airport personnel and show ID card before
passing through the metal detector.

Automatic Implantable
Cardioverter-Defibrillator

Lead placed via the subclavian into the endocardium

Generator is implanted subcutaneously over the pectoralis muscle
Monitors HR/rhythm and identifies ventricular tachycardia &
ventricular fibrillation
Delivers a shock (25 joules) to the heart muscle upon sensing a
lethal arrhythmia
Some newer ICDs are equipped with antitachycardia and
antibradycardia pacers- initiates ovrdrivepacing to prevent painful
shocks

Patient & Family teaching

guide for AICD

Maintain close follow up with physician for testing ICD

function & inspection of site
Medic alert should be worn & information about the ICD
should be available
Watch for signs of infection
Avoid lifting operative side arm above shoulder for about
a week
Avoid direct blows to ICD site

Patient & Family teaching

guide for AICD

When traveling, inform airport official about presence of

AICD
When ICD fires
Routine checks with programmer device needed-2-3
months
Family members should learn CPR
Avoid electromagnetic forces that may turn off device
Participate in ICD support groups