Chp 36 Dysrhythmias

Rhythm Identification and Treatment

Conduction System
Properties of cardiac cells: (Initiate an electrical impulse = muscle contraction)
1) Automoacticity
2) Excitaability
3) Conductivity
4) Contractility

Normal cardiac impluses

Begin SA node -> travel AV node -> through Bundle of His -> ending Purkinje fibers

Nervous Control of the Heart

Autonomic nervous system:
1) Rate of impulse formation
2) Speed of conduction
3) Strength of cardiac contraction
Stimulation of vagus nerve = decrease rate of SA node, slowed impulse conduction AV node,
decrease cardiac muscle contraction.
Stimulation of sympathetic nerves = has the opposite effect

Electrocardiographic Monitoring
ECG- graphic tracing of electrical impulses produced in the heart
Polarized state- (@ rest) inside of the cell is negative compared to outside
Depolarization- inside of the cell positive compared with the outside
Repolarization- restores the cell to polarized state
Phase of cardiac action potential:
1) Phase 0- Upstroke of rapid depolarization
2) Phase 1-3 - Repolarization
3) Phase 4- Polarized
12 ECG: 6 measure frontal plane, 6 measure horizontal plane
Most common lead: II, V1, MCL1
Interpret an ECG:
Lg sq = 25 Sm sq
Sm sq = 0.04 sec horizontally
Lg sq = 0.20 sec horizontally
300 Lg sq = 1 min
Calculate HR:
Most accurate- count the # of QRS complexes in 1 min
If rhythm is regular, simpler process:
1) Count the # R-R intervals in 6 sec and multiply by 10
2) Count sm sq btwn R-R interval divide by 1500
3) Count lg sq btwn R-R interval divide by 300
Calipers used for fine measurements, especially for points of a specific wave/ interval
ECG attached to pt chest, for best contact:
Remove excessive hair
Rub gently w/ dry gauze until slightly pink
Skin oily- alcohol used first
Diaphoretic pt- benzoin applied
Artifact- distortion of the baseline and waveform seen on the ECG
A) Muscle tremor
 B) Loose electrodes

Telemetry Monitoring
Observation of a pt HR & rhythm to rapidly dx dysrhythmias, ischemia, or infarction
Type
1) Centralized monitoring- requires a nurse/ telemetry tech to continuously observe all pt
rhythms at a central location
2) Computerized monitoring- does not require constant surveillance, capability of
detecting & storing data

Assessment of Cardiac Rhythm

Priority is determining underlying cause of dysrhythmias
At all times, the pt, not the “monitor,” must be assessed & treated
Normal sinus rhythm (NSR)- a rhythm that originates in the SA node and follows the normal
conduction pattern of the cardiac cycle
P wave-
PR interval-
QRS complex-
QRS interval-
ST segment-
T wave-
QT interval-

Electrophysiologic Mechanisms of Dysrhythmias

Normally main pacemaker of the heart is the SA node = spontaneously discharges 60-100/mn
Automaticity- able to discharge spontaneously
A pacemaker from another site may be discharged in two ways:
AV node- 40-60/min
Bundle of His- 20-40/min
Excitability- the property of myocardial tissue that allows it to be depolarized by a stimulus
Important- the transmission of the impulse from one fiber to another
Refractory period- the recovery period after stimulation
Absolute refractory phase- occurs when excitability is zero and heart tissue cannot be stimulated
Relative refractory phase- occurs slightly later in the cycle, & excitability is more likely
Full excitability- the heart is completely recovered
Heart blocked- the unblocked areas are activated earlier than the blocked areas

Evaluation of Dysrhythmias
Common causes of dysrhythmias: see Table 36-4 p 847
Systematic approach to assessing a cardiac rhythm: see Table 36-5 p 848
Emergency management: see Table 36-6 p 848
Other methods to evaluate:
Electrophysiologic study (EPS)
Holter monitor
Event monitors
Signal-averaged ECG (SAECG)
Exercise tradmil

Types of Dysrhythmias
Sinus Bradycardia:
Causes:
 Aerobically trainded athletes During sleep
Valsalva maneuver Hypothermia
Increased intraocular pressure Increased vagal tone
Admin parasympathomimetic drugs Hypothyroidism
Increased intracranial pressure Obstrutive jaundice
Inferior wall MI

ECG:
<60 beats/min and regular sinus rhythm

S/S:
Pale, Cool skin Hypotension
Weakness Angina Dizziness/ syncope
SOB Confusion/ disorientation

TX:
Admin atropine for pt w/ symptoms

Sinus Tachycardia
Causes:
Exercise Fever Pain Hypotension Hypovolemia
Anemia Hypoxia Hypoglycemia MI
HF Anxiety Hyperthyroidism Fear

Epinephrine (EpiPen) norepinephrine (Levophed)

atropine (AtroPen Caffeine
theophylline (Theo-Dur) nifedipine (Procardia)
hydralazine (Apresoline)

ECG:
>100 beats/min and regular sinus rhythm

S/S:
Dizziness Dyspnea Hypotension

TX:
Treating underlying cause
Pain- pain management
Treat hypovolemia
IV adenosine (Adenocard) & B-adrenergic blockers- reduce HR & decrease myocardial
oxygen consumption

Drug Alert- Adenosine (Adenocard)

• Monitor pt ECG continuously. Brief period of asytole may be observed
• Observe pt for flushing, dizziness, chest pain, palpitations

Premature Atrail Contraction (PAC)

Contraction originating form an ectopic focus in the atrium in a location other than the
sinus node

Causes:
Emotional stress/ physical fatigue
 Use of caffeine, tobacco, alcohol

ECG:
Usually 60- 100 beats /min & irregular

Clinical significance:
Pt w/ heart disease- indicate enhanced automaticity of the atria/ reentry mechanism

TX:
Depends on pt symptoms
B-Adrenergic blockers- decrease PACs

Paroxysmal Supraventricular Tachycardia (PSVT)

Originating in an ectopic focus anywhere above the bifuracation of the bundle of His

Causes:
Normal heart- overexertion emotional stress deep inspiration
stimulants- caffeine & tobacco
Rheumatic heart disease
Digitalis toxicity
CAD
Cor pumonale

ECG:
100-300 beats/min & regular

S/S:
Prolonged episode & HR >180 beats/min - decreased CO = hypotension, dyspnea,
angina

TX:
Valsalva & coughing
IV adenosine (drug of choice)

Atrial Flutter
An atrial tachydysrhythmia identified by recurring, regular, sawtooth-shaped flutter (F)
waves that originate froma a single ectopic focus in the right atrium

Causes:
CAD Hypertension Mitral valve disorders
Pumonary embolus Chronic lung disease Cor pulmonale
Cardiomyopathy Hyperthyroidism
Digoxin Quinidine Epinephrine

ECG:
Atrial: 250-350 beats/min & regular
Ventricular: > or <100 beats/min & may be regular/ irregular

S/S:
Decrease CO = lead to HF
Increased risk Stroke
 Warfarin (Comadin)- used to prevent stroke pt w/ atrial flutter of >48 hrs duration

TX:
Primary goal- slow the ventricular response by increasing AV block
Ca channel blocker & B-adrenergic blockers
Electrical cardioversion

Atrial Fibrillation
Characterized by a total disorganization of atrial electrical activity due to multiple ectopic
foci resulting in loss of effective atrail contraction

Most common
Prevalence increase with age

Causes:

Pt w/ underlying heart disease

CAD Rheumatic heart disease Cardiomyopathy
HF Hypertensive heart disease Pericarditis

ECG:
Atrial: 350-600 beats/min & irregular
Ventricular: > or <100 beats/min & irregular

S/S:
Decrease in CO
Thrombus
Embolus
Risk for stroke

TX:
Priority- control ventricular rate
Ca channel blocker, B-adrenergic blocker, digoxin
Cardioversion
Antidysrhythmia drugs
If cardioversion or drugs do not work- long term anticoagulation therapy (Warfarin
- drug of choice)
Radiofrequency catheter ablation & Maze procedure

Junctional Dysrhythmias
Dysrhythmias that originate in the area of the AV node, due to SA node failed to fire/
signal block. AV node becomes the pacemaker.

Causes:
CAD Cardiomyopathy Electrolyte imbalances
HF Inferior MI Rheumatic heart disease

ECG:
40-140 beats/min & regular
P wave- inverted, may be hidden in QRS complex
 S/S:
Reduction CO- hemodynamically unstable (hypotensive)

TX:
Pt has symptoms- atropine
Digoxin toxicity- withhold digoxin
B-adrenergic blocker, Ca channel blockers, amiodarone- control rate
DC cardioversion- not be used

First-Degree AV Block
Type of AV block in which every impulse is conducted to the ventricles but the duration of
AV conduction is prolonged
Causes:
MI Rheumatic fever Hyperthyroidism Vagal stimulation
CAD Digoxin B-adrenergic blocker Ca channel blockers
Flecainide

ECG:
Normal & regular
PR interval: >0.20 sec

S/S:
Asymptomatic

TX:
NO treatment

Second-Degree AV Block Type 1

A prolonged AV conduction time until an atrial impulse is non-conducted and a ORS
complex is blocked

Causes:
Digoxin B-adrenergic blocker CAD

ECG:
Atrial: Normal & regular
Ventricular: Slower & irregular
PR interval: progressive lengthening
QRS complex: normal width w/ pattern of 1 non-conducted QRS complex

S/S:
Result of MI/ infarction
Warning signal- AV conduction signal

TX:
Symptomatic- Atropine
Temporary pacemaker
Bardycardia become symptomatic when one or more are present:
1. Hypotension
2. HF
3. Shock
 Asymptomatic- Closely observed w/ transcutaneous pacemaker on standby

Second-Degree AV Block Type 2

Block in one of the bundle branches is present

Causes:
Rheumatic heart disease Anterior MI Digitalis toxicity CAD

ECG:
Atrial: Usually normal & regular
Ventricular: Slower & irregular
P wave: more P waves than QRS complexes
PR interval: Normal or prolonged
QRS complexes: Widened QRS, preceded by 2 or more P waves, w/ nonconducted QRS
complexes
S/S:
Often progress to third-degree w/ poor prognosis
Decreased Co w/ subsequent hypotension & MI
Indication: permanent pacemaker

TX:
Temporary tx if pt becomes symptomatic
Temporary transvenous or transcutaneous pacemaker

Third-Degree AV Block
Complete heart block
Constitutes one form of AV dissociation in which no impulses from the atria are
conducted to the ventricless

Clinical association:
Severe heart disease- CAD, MI, myocarditis, cardiomyopathy
Systemic diseases- amyloidosis, progressive systemic sclerosis
Digoxin, B-adrenergic blockers, Ca channel blockers

ECG:
Atrial: Regular but may appear irregular
Ventricular: 20-40 beats/min & regular
PR interval- Variable
QRS complex- Normal/ widened, no relationship w/ P waves

Clinical significance:
Reduced CO w/ subsequent ischemia, HF, shock

TX:
Symptomatic- transcutaneous pacemaker until temporary transvenous pacemaker
inserted
Atropine, epinephrine, isoproterenol, dopamine- temporary measures
Need permanent pacemaker ASAP

Premature Ventricular Contractions (PVC)

Contraction origination in an ectopic focus in the ventricles
 Clinical association:
Stimulants Exercise Emotional stress
Electrolyte imbalances Hypoxia Fever
Mitral valve prolapse MI HF
CAD

ECG:
Regular/ irregular
P wave: not usually visible
PR interval: not measurable
QRS complexes: Wide & distorted

Clinical significance:
In heart disease- reduce CO & precipitate angina & HF
IMPORTANT: apical-radial pulse rate

TX:
Often based on the cause

Ventricular Tachycardia (VT)

Dx is make when a run of 3 or more PVCs occurs
Occurs when an ectopic focus or foci fire repetitively & ventricle takes control as the
pacemaker

Clinical association:
MI Significant electrolyte imbalances Mitral valve prolapse
CAD Cardiomopathy Long QT syndrom
CNS disorders Digitalis toxicity No evidence of cardiac disease

ECG:
150-250 beats/min & regular/irregular
P wave- not usually visible
PR interval: not measurable
QRS complexes: Wide & distorted

Clinical significance:
Severe decrease in CO
Hypotension Pulmonary edema Decreased cerebral blood flow
Cardiopulmonary arrest

TX:
Precipitating causes must be identified & treated
Monomorphic & hemodynamically stable- IV procainamide, sotalol, amiodarone, lidocaine
Hemodynamically unstable- IV amiodoarone/ lidocaine followed by cardioversion
Polymorphic w/ normal baseline QT interval- B-adrenergic blocker, lidocaine,
amiodarone, procainamide, sotalol
Polymorphic w/ prolonged baseline QT interval- IV magnesium, isoproternol, phenytoin,
lidocaine, antitachycardia pacing
W/o pulse- CPR & rapid defibrillation

Ventricular Febrillation
 Mechanically the ventricle is simply “quivering” & no effective contraction & consequently
no CO, occurs

Clinical association:
Acute MI MI Cardiomyopathy Accidental electric shock
Acidosis CAD Coronary reperfusion Cardiac pacing/cardiac catheterization
Hyperkalemia Hypoxemia Drug toxicity

ECG:
HR not measurable & irregular
P wave- absent
PR interval & QRS complex- not measurable

Clinical significance:
Unresponsive Pulseless Apneic state

TX:
CPR & ACLS
Defibrillation & definitive drug therapy

Asystole
Represents the total absence of ventricular electrical activity
Pt unresponsice, pulselesss, apneic

Clinical association:
Advanced cardiac disease
Severe cardiac conduction system disturbance
End-stage HF

Clinical significance:
End-stage cardiac disease or had a prolonged arrest & cannot be resuscitated

TX:
CPR w/ initiation of ACLS measures (intubation, transcutaneous pacing, IV epinephrine &
atropine)

Pulseless Electrical Activity (PEA)

A situation in which electrical activity can be observed on the ECG, but there is no
mechanical activity of the ventricles and the pt has no pulse
Causes:
Hypovolemia Hyperkalemia/ Hypokalemia Metabolic acidosis
Hypoxia Drug overdose Pulmonary embolus
MI Cardiac tamponade Tension pneumothorax
Hypothermia
Tx:
CPR followed by intubation & IV therapy w/ epinephrine
Correct underlying cause

Sudden Cardiac Death (SCD)

Refers to death from a cardiac cause
Cause:
 Ventricular dysrhythmias
Specifically ventricular tachycardia/ fibrillation

Prodysrhythmia
Antidysrhythmia drugs may cause life threatening dysrhythmias similar to those for which
they are administered
Causes:
Severe left ventricular dysfunction
Digoxin & class IA, IC, III antidysrhythmia drugs
First day most susceptible

Antidysrhythmia Durgs
See Table 36-8 p 856

Defibrillation
Most effective in terminating ventricular fibrillation & pulseless VT
Deliver energy using:
Monophasic defibrillators- one direction
Biphasic defibrillators- two directions
After initial shock, CPR started immediately beginning w/ chest compressions
Manual defibrillators- require to interpret cardiac rhythm, determine need, deliver shock
Automatic external defibrillators (AED)- has rhythm detection capability, advise the operator to
deliver shock
General steps to defibrillation:
1) CPR in progress until defibrillator available
2) Defibrillator turned on & proper energy selected
3) Synchronizer switch turned off
Conductive materials- one on R of sternum just below the clavicle, other L of the apex
Operator call “all clear” (not touching pt or bed)
Charge delivered, depressing buttons simultaneously

Synchornized Cardioversion
Choice for unstable ventricular/ supraventricular tachydysrhythmias
Synchronizer switch ON
Procedure same as defibrillation w/ the following exceptions:
Nonemergency basis- pt sedated before (IV midazolam [Versad])
Supraventricular tachycardia/ VT with a pulse- ASAP
Energy started 50 joules monophasic defibrillator and increased as needed

Implantable Cardioverter-Defibrillator (ICD)

For pt who:
1) Survived SCD
2) Have spontaneous sustained VT
3) Have syncope w/ inducible ventricular tachycardia/fibrillation during EPS
4) @ high risk for future life-threatening dysrhythmias
A battery-powered pulse denerator is implanted subq, usually over pectoral muscle on
the pt nondominant side
Monitor HR & rhythms
Approx 25 after detecting a lethal dysrhythmia, deliver 25-joule or less shock
First shock unsuccessful, recycles & cont to deliver shocks
Education IMPORTANT see Table 36-9 p 858
Support groups & online resources
Pacemaker
Cardiac pacemaker- an electronic device used to pace the heart when the normal conduction
pathway is damaged/ diseased
Permanent pacemaker- implanted totally w/in the body
Implanted subq, over pectoral muscle on the pt nondominant side
Indications for Permanent Pacemaker Therapy see Table 36-10 p 859
Cardiac resynchronization therapy (CRT)- a pacing technique that resynchronizes the cardiac
cycle by pacing both ventricles, thus promoting improvement in ventricular function

Temporary Pacemaker
Power source outside the body
Indications for Temporary Pacing see Table 36-11 p 859
3 Types of Temp Pacemaker:
Transvenous pacemaker- inserted in critical care unit in emergency situation
Used until permanent pacemaker inserted or underlying cause
been resolved
Epicardial pacing- inserted during heart surgery
Placed prophylactically
Transcutaneous pacemaker (TCP)- used to provide adequate HR & rhythm in pt
emergency situation
Noninvasive procedure
Before initiation, important to tell pt:
Uncomfortable muscle contractions
Reassure therapy is temp
Analgesia and/or sedation should be provided

Patient Monitoring
Failure to sense- occurs when the pacemaker fails to recognize spontaneous atrial or
ventricular activity, and it fires inappropriately
Caused: pacer lead damage, battery failure, dislodgement of the electrode
Failure to capture- occurs when the electrical charge to the myocardium is insufficient to
produce atrial or ventricular contraction
Caused: pacer lead damage, battery failure, dislodgement of the electrode,
fibrosis at the electrode tip
Prevent or assess for complications:
Prophylactic IV antibiotic therapy before & after insertion
Postinsertion chest x-ray
Observation insertion site
Continuous ECG monitoring
Arm & shoulder activity limited
Temperature elevation noted & pain treated
Pt and family teaching guide see Table 36-12 p 861
GOAL of pacemaker therapy- to enhance physiologic functioning and the quality of life
After discharge, pacemaker checked regular basis

Radiofrequency Catheter Ablation Therapy

Radiofrequency energy is used to “burn” or ablate areas of the conduction system
Tx of tachydysrhythmias
When done pt must have permanent pacemaker inserted at the same time
Low complication rate
Care similar to cardiac catheterization
ECG Changes Associated with Acute Coronary Syndrome
Primary diagnostic tool
see Table 36-13 p 861
Ischemia
ST segment depression and/or T wave inversion
Occurs in response to the electrical disturbance in the myocardial cells due to an inadequate
supply of blood and oxygen

Injury and Infarction

ST segment elevation
Serum cardiac markers present- infarction has occurred referred to ST-segment-elevation MI
Pathologic Q wave- if it appears it indicates that a last half the thickness of the heart wall is
involved, referred to Q wave MI
T wave inversion- occurs w/in hrs following injury & persist for months
ECG changes- due to a prolonged lack of blood & oxygen leading to necrosis

Syncope
A brief lapse in consciousness accompanied by a loss in postural tone (fainting
Most common cardiovascular causes:
1) Neurocardiogenic syncope or “vasovagal” syncope
2) Primary cardiac dysrhythmias
Noncardiovascular causes:
1) hypoglycemia
2) Hysteria
3) Unwitnessed seizure
4) Vertebrobasilar transient ischemic attack
Diagnostic:
Echocardiography & stress testing
EPS
Head-upright tilt-table testing:
In pt w/out structural heart disease or in whom EPS testing is not diagnostic
Test positive- slight increase in HR & diastolic BP, & slight decrease in systolic BP
Holter monitors & event monitors