Transcript Basic Dysrhythmia Interpretation

Basic Dysrhythmia
Interpretation
NURS 108
Spring 2008
Majuvy L. Sulse RN, MSN,CCRN
Cardiac Cycle
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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
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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)
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CO= SV XHR
Cardiac Cycle
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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
STARLING’S 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
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Sympathetic-prepares for physical activity-fight or
flight response-norepinephrine (Adrenergic nerve
endings)
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Alpha-vasoconstriction
Beta
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Beta 1-increase HR & contractility
Beta 2-bronchial dilation & vasodilation
Parasympathetic-rest & digest function
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Acetylcholine (cholinergic nerve endings)
Electrophysiologic Properties
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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
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3 major cations
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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
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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
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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
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SA node (60-100bpm)
Internodal pathways
AV node ( 40-60bpm)
Bundle of His
Bundle Branches
Purkenje networks (20-40bpm)
EKG
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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
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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
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Limb leads
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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
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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
interval-0.12-0.20(time for atrial depolarization-AV nodePurkenje 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
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6 second method
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P-P or R-R interval method
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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
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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
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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
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Waveforms outside the heart-interference caused by:
 Patient movement wandering baseline
 Loose or defective electrodes-lost contact with
patient’s 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
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Causes:
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Adverse effects:
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Vagal stimulation, MI, hypoxia
Digitalis toxicity
Medication side effects
Normal to athletes
Dizziness, weakness, syncope, diaphoresis, pallor,
hypotension
Treatment
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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
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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
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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
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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
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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)
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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
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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
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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
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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
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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)
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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
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Myocardial ischemia, Emotional stress, increased physical exertion,
CHF, electrolyte imbalance, digitalis toxicity or acid base imbalances
Treatment- based on symptoms and causative factors
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O2 and antidysrhythmics
PVCs
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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
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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)
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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
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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
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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
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Prolonged PR interval that results from a delay in the AV
node’s 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
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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
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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)
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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
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Device that substitutes for the normal pacemaker of the heart’s
electrical conduction system
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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
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Temporary-used to sustain HR in an emergency situation
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Transcutaneous (TCP)-external cardiac pacing
Transvenous-lead wire threaded through the skin into a large vein
Permanent- implanted in patient’s chest
Indications for insertion of
Pacemakers
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Temporary
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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-
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Chronic atrial fibrillation with slow ventricular response
Fibrotic or sclerotic changes in the cardiac conduction system
Sick sinus syndrome or Sinus node dysfunction
Tachyarrhythmias
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Symptomatic bradycardia and Third degree AV block not
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responding to pharmacologic interventions
Permanent Pacemakers
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Atrial- lead wire inserted into the Right atrium-stimulates the
atrium then travels down the electrical conduction through the
ventricles
Permanent Pacemakers
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Ventricular- lead wire inserted into the Right ventricle.
The electrical impulse from the pacemaker generator
produces ventricular depolarization
Permanent Pacemakers
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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
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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
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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
person’s heart beats
 O-none
 T-triggered
 D-dual
Code System
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4th letter- ability of generator to be programmed
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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
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P-Antitachycardia
S-Shock
D-antitachycardia processing & shock
O-none
Common Problems associated with
Pacemakers
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Battery failure
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Decreased amplitude of pacemaker spike and a slowing
pacemaker rate
Immediate transport to the hospital depending on the
patient’s symptoms or underlying rhythm
Runaway Pacemakers
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Rapid rate of electrical impulse discharge results
Immediate transport to a hospital
Failure to Sense
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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
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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
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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
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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
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Consent
VS
Skin prep
Pre-op checklist-NPO, dentures, pins
Position post op is important
Maintain hemodynamic stability
Prevent complications
Patient & family Teaching Guides
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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
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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
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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 CardioverterDefibrillator
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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
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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
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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