Definition of Arrhythmia:

The Origin, Rate, Rhythm,

Conduct velocity and sequence
of heart activation are
abnormally.
Anatomy of the conducting system
Arrhythmia Presentation
Palpitation.
Dizziness.
Chest Pain.
Dyspnea.
Fainting.
Sudden cardiac death.
Pathogenesis and Inducement
of Arrhythmia
Some physical condition
Pathological heart disease
Other system disease
Electrolyte disturbance and
acid-base imbalance
Physical and chemical factors
or toxicosis
Mechanism of
Arrhythmia
Abnormal heart pulse
formation
1. Sinus pulse
2. Ectopic pulse
3. Triggered activity
Abnormal heart pulse
conduction
1. Reentry
2. Conduct block
Classification of
Arrhythmia
Abnormal heart pulse formation
1. Sinus arrhythmia
2. Atrial arrhythmia
3. Atrioventricular junctional
arrhythmia
4. Ventricular arrhythmia
Abnormal heart pulse conduction
1. Sinus-atrial block
2. Intra-atrial block
3. Atrio-ventricular block
4. Intra-ventricular block
Abnormal heart pulse formation
and conduction
Diagnosis of
Arrhythmia
Medical history
Physical examination
Laboratory test
Therapy Principal
Pathogenesis therapy
Stop the arrhythmia
immediately if the
hemodynamic was unstable
Individual therapy
Anti-arrhythmia
Agents
Anti-tachycardia agents
Anti-bradycardia agents
 Anti-tachycardia
agents
Modified Vaugham Williams
classification
1. I class: Natrium channel blocker
2. II class: -receptor blocker
3. III class: Potassium channel blocker
4. IV class: Calcium channel blocker
5. Others: Adenosine, Digital
Anti-bradycardia
agents
1. -adrenic receptor activator
2. M-cholinergic receptor blocker
3. Non-specific activator
Clinical usage
Anti-tachycardia agents:
Ia class: Less use in clinic
1. Guinidine
2. Procainamide
3. Disopyramide: Side effect: like M-
cholinergic receptor blocker
Anti-tachycardia agents:
Ib class: Perfect to
ventricular tachyarrhythmia
1. Lidocaine
2. Mexiletine
Anti-tachycardia agents:
Ic class: Can be used in ventricular
and/or supra-ventricular
tachycardia and extrasystole.
1. Moricizine
2. Propafenone
Anti-tachycardia
agents:
II class: -receptor blocker
1. Propranolol: Non-selective
2. Metoprolol: Selective 1-
receptor blocker, Perfect to
hypertension and coronary
artery disease patients
associated with
tachyarrhythmia.
Anti-tachycardia
agents:
III class: Potassium channel
blocker, extend-spectrum anti-
arrhythmia agent.
Amioarone: Perfect to coronary
artery disease and heart failure
patients
Sotalol: Has -blocker effect
Bretylium
Anti-tachycardia
agents:
IV class: be used in
supraventricular tachycardia
1. Verapamil
2. Diltiazem
Others:
Adenosine: be used in
supraventricular tachycardia
Anti-bradycardia
agents
Isoprenaline
Epinephrine
Atropine
Aminophylline
Proarrhythmia effect of
antiarrhythmia agents
Ia, Ic class: Prolong QT interval,
will cause VT or VF in coronary
artery disease and heart failure
patients
III class: Like Ia, Ic class agents
II, IV class: Bradycardia
Non-drug therapy

Cardioversion: For tachycardia

especially hemodynamic unstable
patient
Radiofrequency catheter ablation
(RFCA): For those tachycardia
patients (SVT, VT, AF, AFL)
Artificial cardiac pacing: For
bradycardia, heart failure and
malignant ventricular arrhythmia
patients.
Sinus Arrhythmia
Sinus tachycardia
Sinus rate > 100 beats/min (100-180)
Causes:
1. Some physical condition: exercise,
anxiety, exciting, alcohol, coffee
2. Some disease: fever,
hyperthyroidism, anemia,
myocarditis
3. Some drugs: Atropine, Isoprenaline
Neednt therapy
SINUS TACHYCARDIA
Rate: 101-160/min
P wave: sinus
QRS: normal
Conduction: normal
Rhythm: regular or slightly irregular
The clinical significance of this dysrhythmia depends on the
underlying cause. It may be normal.
Underlying causes include:
increased circulating catecholamines
CHF
hypoxia
PE
increased temperature
stress
response to pain
Treatment includes identification of the underlying cause and
correction.
 Sinus Bradycardia
Sinus rate < 60 beats/min
Normal variant in many normal and older
people
Causes: Trained athletes, during sleep, drugs
(-blocker) , Hypothyriodism, CAD or SSS
Symptoms:
1. Most patients have no symptoms.
2. Severe bradycardia may cause dizziness,
fatigue, palpitation, even syncope.
Neednt specific therapy, If the patient has
severe symptoms, planted an pacemaker may
be needed.
SINUS BRADYCARDIA
Rate: 40-59 bpm
P wave: sinus
QRS: Normal (.06-.12)
Conduction: P-R normal or slightly prolonged at slower rates
Rhythm: regular or slightly irregular
This rhythm is often seen as a normal variation in athletes, during
sleep, or in response to a vagal maneuver. If the bradycardia
becomes slower than the SA node pacemaker, a junctional rhythm
may occur.
Treatment includes:
treat the underlying cause,
atropine,
isuprel, or
artificial pacing if patient is hemodynamically
compromised.
SINUS ARRHYTHIMIA
Rate: 45-100/bpm
P wave: sinus
QRS: normal
Conduction: normal
Rhythm: regularly irregular
The rate usually increases with inspiration and decreases with
expiration.
This rhythm is most commonly seen with respiration due to
fluctuations in vagal tone.
The non respiratory form is present in diseased hearts and
sometimes confused with sinus arrset (also known as "sinus
pause").
Treatment is not usually required unless symptomatic bradycardia
is present.
WANDERING PACEMAKER
Rate: variable depending on the site of the pacemaker; usually 45-
100/ bpm.
P wave: also variable in morphology
QRS: normal
Conduction: P-R interval varies depending on the site of the
pacemaker
Rhythm: irregular
This dysrhythmia may occur in normal hearts as a result of
fluctuations in vagal tone. It may also be seen in patients with heart
disease or COPD.
Wandering atrial pacemaker may also be a precursor to multifocal
atrial tachycardia.
There is usually no treatment required.
 Sinus Arrest or Sinus
Standstill
Sinus arrest or standstill is recognized
by a pause in the sinus rhythm.
Causes: myocardial ischemia, hypoxia,
hyperkalemia, higher intracranial
pressure, sinus node degeneration and
some drugs (digitalis, -blocks).
Symptoms: dizziness, amaurosis,
syncope
Therapy is same to SSS
SINUS PAUSE, ARREST
Rate: normal
P wave: those that are present are normal
QRS: normal
Conduction: normal
Rhythm: The basic rhythm is regular. The length of the pause is
not a multiple of the sinus interval.
This may occur in individuals with healthy hearts. It may also
occur with increased vagal tone, myocarditis, MI, and digitalis
toxicity.
If the pause is prolonged, escape beats may occur.
The treatment of this dysrhythmia depends on the underlying
cause.
If the cause is due to increased vagal tone and the patient is
symptomatic, atropine may be indicated.
Sinoatrial exit block
(SAB)
SAB: Sinus pulse was blocked
so it couldnt active the atrium.
Causes: CAD, Myopathy,
Myocarditis, digitalis toxicity,
et al.
Symptoms: dizziness, fatigue,
syncope
Therapy is same to SSS
SINOATRIAL BLOCK
Rate: normal or bradycardia
P wave: those present are normal
QRS: normal
Conduction: normal
Rhythm: basic rhythm is regular.
In a type I SA block, the P-P interval shortens until one P wave is
dropped.
In a type II SA block, the P-P intervals are an exact multiple of the
sinus cycle, and are regular before and after the dropped P wave.
This usually occurs transiently and produces no symptoms. It may
occur in healthy patients with increased vagal tone. It may also be
found with CAD, inferior MI, and digitalis toxicity.
Sinoatrial exit block
(SAB)
Divided into three types: Type
I, II, III
Only type II SAB can be
recognized by EKG.
Sick Sinus Syndrome
(SSS)
SSS: The function of sinus node was
degenerated. SSS encompasses both
disordered SA node automaticity and
SA conduction.
Causes: CAD, SAN degeneration,
myopathy, connective tissue disease,
metabolic disease, tumor, trauma and
congenital disease.
With marked sinus bradycardia, sinus
arrest, sinus exit block or junctional
escape rhythms
Bradycardia-tachycardia syndrome
 Sick Sinus Syndrome
(SSS)
EKG Recognition:
1. Sinus bradycardia, 40 bpm;
2. Sinus arrest > 3s
3. Type II SAB
4. Nonsinus tachyarrhythmia ( SVT, AF
or Af).
5. SNRT > 1530ms, SNRTc > 525ms
6. Instinct heart rate < 80bmp
Sick Sinus Syndrome
(SSS)
Therapy:
1. Treat the etiology
2. Treat with drugs: anti-
bradycardia agents, the effect
of drug therapy is not good.
3. Artificial cardiac pacing.
Atrial arrhythmia
Premature contractions
The term premature
contractions are used to
describe non sinus beats.
Common arrhythmia
The morbidity rate is 3-5%
Atrial premature contractions
(APCs)
APCs arising from somewhere in either the
left or the right atrium.
Causes: rheumatic heart disease, CAD,
hypertension, hyperthyroidism, hypokalemia
Symptoms: many patients have no
symptom, some have palpitation, chest
incomfortable.
Therapy: Neednt therapy in the patients
without heart disease. Can be treated with
-blocker, propafenone, moricizine or
verapamil.
PREAMATURE ATRIAL
CONTRACTIONS
Rate: normal or accelerated
P wave: usually have a different morphology than sinus P waves
because they originate from an ectopic pacemaker
QRS: normal
Conduction: normal, however the ectopic beats may have a
different P-R interval.
Rhythm: PAC's occur early in the cycle and they usually do not
have a complete compensatory pause.
PAC's occur normally in a non diseased heart.
However, if they occur frequently, they may lead to a more serious
atrial dysrhythmias.
They can also result from CHF, ischemia and COPD.
 Atrial tachycardia

Classify by automatic atrial tachycardia

(AAT); intra-atrial reentrant atrial
tachycardia (IART); chaotic atrial
tachycardia (CAT).
Etiology: atrial enlargement, MI;
chronic obstructive pulmonary disease;
drinking; metabolic disturbance;
digitalis toxicity; electrolytic
disturbance.
Atrial tachycardia

May occur transient; intermittent;

or persistent.
Symptoms: palpitation; chest
uncomfortable, tachycardia may
induce myopathy.
Auscultation: the first heart sound
is variable
Intra-atrial reentry
tachycardia (IART)
ECG characters:
1. Atrial rate is around 130-150bpm;
2. P wave is different from sinus P wave;
3. P-R interval 0.12
4. Often appear type I or type II, 2:1 AV
block;
5. EP study: atrial program pacing can
induce and terminate tachycardia
 Automatic atrial
tachycardia (AAT)
ECG characters:
1. Atrial rate is around 100-200bpm;
2. Warmup phenomena
3. P wave is different from sinus P
wave;
4. P-R interval 0.12
5. Often appear type I or type II, 2:1 AV
block;
6. EP study: Atrial program pacing cant
induce or terminate the tachycardia
 Chaotic atrial tachycardia
(CAT)
Also termed Multifocal atrial
tachycardia.
Always occurs in COPD or CHF,
Have a high in-hospital mortality ( 25-
56%). Death is caused by the severity of
the underlying disease.
ECG characters:
1. Atrial rate is around 100-130bpm;
2. The morphologies P wave are more than
3 types.
3. P-P, P-R and R-R interval are different.
4. Will progress to af in half the cases
5. EP study: Atrial program pacing cant
induce or terminate the tachycardia
 Therapy
IRAT: Esophageal Pulsation
Modulation, RFCA, Ic and IV class
anti-tachycardia agents
AAT: Digoxin, IV, II, Ia and III class
anti-tachycardia agents; RFCA
CAT: treat the underlying disease,
verapamil or amiodarone.
Associated with SSS: Implant pace-
maker.
PAROXYSMAL ATRIAL
TACHYCARDIA
Rate: atrial 160-250/min: may conduct to ventricles 1:1, or 2:1,
3:1, 4:1 into the presence of a block.
P wave: morphology usually varies from sinus
QRS: normal (unless associated with aberrant ventricular
conduction).
Conduction: P-R interval depends on the status of AV conduction
tissue and atrial rate: may be normal, abnormal, or not measurable.
PAT may occur in the normal as well as diseased heart.
It is a common complication of Wolfe-Parkinson-White syndrome.

This rhythm is often transient and doesn't require treatment.

However, it can be terminated with vagal maneuvers.
Digoxin, antiarrhythmics, and cardioversion may be used.
Atrial flutter
Etiology:
1. It can occur in patients with
normal atrial or with abnormal
atrial.
2. It is seen in rheumatic heart
disease (mitral or tricuspid valve
disease), CAD, hypertension,
hyperthyroidism, congenital heart
disease, COPD.
3. Related to enlargement of the atria
4. Most AF have a reentry loop in
right atrial
Atrial flutter
Symptoms: depend on
underlying disease, ventricular
rate, the patient is at rest or is
exerting
With rapid ventricular rate:
palpitation, dizziness,
shortness of breath, weakness,
faintness, syncope, may
develop angina and CHF.
Atrial flutter
Therapy:
1. Treat the underlying disease
2. To restore sinus rhythm:
Cardioversion, Esophageal
Pulsation Modulation, RFCA,
Drug (III, Ia, Ic class).
3. Control the ventricular rate:
digitalis. CCB, -block
4. Anticoagulation
 Atrial fibrillation
Subdivided into three types:
paroxysmal, persistent, permanent.
Etiology:
1. Morbidity rate increase in older
patients
2. Etiology just like atrial flutter
3. Idiopathic
Mechanism:
1. Multiple wavelet re-entry;
2. Rapid firing focus in pulmonary vein,
vena cava or coronary sinus.
ATRIAL FIBRILLATION
Rate: atrial rate usually between 400-650/bpm.
P wave: not present; wavy baseline is seen instead.
QRS: normal
Conduction: variable AV conduction; if untreated the ventricular
response is usually rapid.
Rhythm: irregularly irregular. (This is the hallmark of this
dysrhythmia).
Atrial fibrillation may occur paroxysmally, but it often becomes
chronic. It is usually associated with COPD, CHF or other heart
disease.
Treatment includes:
Digoxin to slow the AV conduction rate.
Cardioversion may also be necessary to terminate this rhythm.
 Atrial fibrillation
Manifestation:
Affected by underlying diseases, ventricular
rate and heart function.
May develop embolism in left atrial. Have
high incidence of stroke.
The heart rate, S1 and rhythm is irregularly
irregular
If the heart rhythm is regular, should
consider about (1) restore sinus rhythm; (2)
AF with constant the ratio of AV conduction;
(3) junctional or ventricular tachycardia; (4)
slower ventricular rate may have complete
AV block.
Atrial fibrillation
Therapy:
1. Treat the underlying disease
2. Restore sinus rhythm: Drug,
Cardioversion, RFCA, Maze
surgery
3. Rate control: digitalis. CCB, -
block
4. Antithrombotic therapy:
Aspirine, Warfarin
 Atrioventricular
Junctional arrhythmia
Atrioventricular junctional
premature contractions

Etiology and manifestation is

like APCs
Therapy the underlying disease
Neednt anti-arrhythmia therapy.
PREMATURE JUNCTIONAL
CONTRACTION
Rate: normal or accelerated.
P wave: as with junctional rhythm.
QRS: normal
Conduction: P-R interval < .12 secs if P waves are
present.
Rhythm: PJC's occur early in the cycle of the baseline
rhythm. A full compensatory pause may occur.
PJCs may occur in both healthy and diseased hearts. If
they are occasional, they are insignificant. If they are
frequent, junctional tachycardia may result.
Treatment is usually not required.
JUCTIONAL TACHYCARDIA
Rate: faster than 60/bpm
P wave: as with junctional rhythm.
QRS: normal or widened with aberrant ventricular conduction.
Conduction: P-R interval usually < .12 seconds if present
Rhythm: usually regular
The clinical significance of this rhythm depends upon the basic
rhythm disturbance. If the ventricular rate is rapid, cardiac output
may decrease.
Treatment includes:
finding and correcting the underlying cause,
vagal maneuvers,
verapamil, and
cardioversion.
Nonparoxysmal AV junctional
tachycardia
Mechanism: relate to hyper-
automaticity or trigger activity of AV
junctional tissue
Etiology: digitalis toxicity; inferior
MI; myocarditis; acute rheumatic
fever and postoperation of valve
disease
ECG: the heart rate ranges 70-150
bpm or more, regular, normal QRS
complex, may occur AV dissociation
and wenckebach AV block
Nonparoxysmal AV junctional
tachycardia

Therapy:
Treat underlying disease;
stopping digoxin, administer
potassium, lidocaine, phenytoin
or propranolol.
Not for DC shock
It can disappear spontaneously. If
had good tolerance, not require
therapy.
JUNCTIONAL ESCAPE RHYTHM
Rate: 40-60/bpm
P wave: inverted in leads where they are normally upright; this
happens when the atrial depolarization wave moves towards a
negative (-) lead.P waves may occur before, during or after the QRS,
depending on where the pacemaker is located in the AV junction .
QRS: normal
Conduction: P-R interval < .12 seconds if present.
Rhythm: irregular as a result of the escape beats.
The most common cause of this rhythm in healthy individuals is sinus
bradycardia.
It may also be seen in the presence of a high degree or complete AV
block. If the ventricular rate is slow, hemodynamic compromise may
occur.
Treatment depends upon the underlying cause and the baseline
dysrhythmias.
Atropine or a pacemaker may be used to increase
the ventricular rate.
Paroxysmal tachycardia
Most PSVT (paroxysmal supraventricular
tachycardia) is due to reentrant
mechanism.
The incidence of PSVT is higher in AVNRT
(atrioventricular node reentry tachycardia)
and AVRT (atioventricular reentry
tachycardia), the most common is AVNRT
(90%)
Occur in any age individuals, usually no
structure heart disease.
Paroxysmal tachycardia
Manifestation:
Occur and terminal abruptly.
Palpitation, dizziness,
syncope, angina, heart failure
and shock.
The sever degree of the
symptom is related to
ventricular rate, persistent
duration and underlying
disease
Paroxysmal tachycardia
ECG characteristic of AVNRT
1. Heart rate is 150-250 bpm, regular

2. QRS complex is often normal, wide

QRS complex is with aberrant
conduction
3. Negative P wave in II III aVF, buried
into or following by the QRS
complex.
4. AVN jump phenomena
Paroxysmal
tachycardia
ECG characteristic of AVRT
1. Heart rate is 150-250 bpm,
regular
2. In orthodromic AVRT, the QRS
complex is often normal, wide
QRS complex is with antidromic
AVRT
3. Retrograde P wave, R-
P>110ms.
Paroxysmal
tachycardia
Therapy:
AVNRT & orthodromic AVRT
1. Increase vagal tone: carotid sinus
massage, Valsalva maneuver.if no
successful,
2. Drug: verapamil, adrenosine,
propafenone
3. DC shock
Antidromic AVRT:
1. Should not use verapamil, digitalis, and
stimulate the vagal nerve.
2. Drug: propafenone, sotalol, amiodarone
RFCA
 Pre-excitation
syndrome

(W-P-W
There are syndrome)
several type of accessory
pathway
1. Kent: adjacent atrial and
ventricular
2. James: adjacent atrial and his
bundle
3. Mahaim: adjacent lower part of the
AVN and ventricular
Usually no structure heart disease,
occur in any age individual
WPW syndrome
Manifestation:
Palpitation, syncope, dizziness
Arrhythmia: 80% tachycardia
is AVRT, 15-30% is AFi, 5% is
AF,
May induce ventricular
fibrillation
 WPW syndrome
Therapy:
1. Pharmacologic therapy:
orthodrome AVRT or associated AF,
AFi, may use Ic and III class
agents.
2. Antidromic AVRT cant use digoxin
and verapamil.
3. DC shock: WPW with SVT, AF or Afi
produce agina, syncope and
hypotension
4. RFCA
Ventricular arrhythmia
Ventricular Premature
Contractions (VPCs)
Etiology:
1. Occur in normal person
2. Myocarditis, CAD, valve heart
disease, hyperthyroidism,
Drug toxicity (digoxin,
quinidine and anti-anxiety
drug)
3. electrolyte disturbance,
anxiety, drinking, coffee
VPCs

Manifestation:
1. palpitation
2. dizziness
3. syncope
4. loss of the second heart
sound
 PVCs
Therapy: treat underlying disease,
antiarrhythmia
No structure heart disease:
1. Asymptom: no therapy
2. Symptom caused by PVCs: antianxiety
agents, -blocker and mexiletine to relief
the symptom.
With structure heart disease (CAD, HBP):
1. Treat the underlying diseas
2. -blocker, amiodarone
3. Class I especially class Ic agents should be
avoided because of proarrhytmia and lack
of benefit of prophylaxis
Ventricular
tachycardia
Etiology: often in organic heart
disease
CAD, MI, DCM, HCM, HF,
long QT syndrome
Brugada syndrome
Sustained VT (>30s),
Nonsustained VT
Monomorphic VT, Polymorphic
VT
Ventricular
tachycardia
Torsades de points (Tdp): A special
type of polymorphic VT,
Etiology:
1. congenital (Long QT),
2. electrolyte disturbance,
3. antiarrhythmia drug proarrhythmia
(IA or IC),
4. antianxiety drug,
5. brain disease,
6. bradycardia
Ventricular
tachycardia
Accelerated idioventricular
rhythm:
1. Related to increase automatic
tone
2. Etiology: Often occur in
organic heart disease,
especially AMI reperfusion
periods, heart operation,
myocarditis, digitalis toxicity
 VT
Manifestation:
1. Nonsustained VT with no
symptom
2. Sustained VT : with symptom
and unstable hemodynamic,
patient may feel palpitation,
short of breathness,
presyncope, syncope, angina,
hypotension and shock.
 VT
ECG characteristics:
1. Monomorphic VT: 100-250 bpm, occur and
terminate abruptly,regular
2. Accelerated idioventricular rhythm: a runs
of 3-10 ventricular beats, rate of 60-110
bpm, tachycardia is a capable of warm up
and close down, often seen AV
dissociation, fusion or capture beats
3. Tdp: rotation of the QRS axis around the
baseline, the rate from 160-280 bpm, QT
interval prolonged > 0.5s, marked U wave
 Treatment of VT
1. Treat underlying disease
2. Cardioversion: Hemodynamic
unstable VT (hypotension,
shock, angina, CHF) or
hemodynamic stable but drug
was no effect
3. Pharmacological therapy: -
blockers, lidocain or
amiodarone
4. RFCA, ICD or surgical therapy
 Therapy of Special

type VT
Accelerated idioventricular rhythm:
usually no symptom, neednt
therapy.
Atropine increased sinus rhythm
Tdp:
1. Treat underlying disease,
2. Magnesium iv, atropine or
isoprenaline, -block or pacemaker
for long QT patient
3. temporary pacemaker
Ventricular flutter and
fibrillation
Often occur in severe organic heart
disease: AMI, ischemia heart
disease
Proarrhythmia (especially produce
long QT and Tdp), electrolyte
disturbance
Anaesthesia, lightning strike,
electric shock, heart operation
Its a fatal arrhythmia
Ventricular flutter and
fibrillation
Manifestation:
Unconsciousness, twitch, no
blood pressure and pulse,
going to die
Therapy:
1. Cardio-Pulmonary Resuscitate
(CPR)
2. ICD
Cardiac conduction
block
Block position:
Sinoatrial; intra-atrial;
atrioventricular; intra-
ventricular
Block degree
1. Type I: prolong the conductive
time
2. Type II: partial block
3. Type III: complete block
Atrioventricular Block
AV block is a delay or failure in
transmission of the cardiac impulse
from atrium to ventricle.
Etiology:
Atherosclerotic heart disease;
myocarditis; rheumatic fever;
cardiomyopathy; drug toxicity;
electrolyte disturbance, collagen
disease, levs disease.
AV Block

AV block is divided into three

categories:
1. First-degree AV block
2. Second-degree AV block: further
subdivided into type I and type II
3. Third-degree AV block: complete
block
 AV Block
Manifestations:
First-degree AV block: almost no
symptoms;
Second degree AV block: palpitation,
fatigue
Third degree AV block: Dizziness, agina,
heart failure, lightheadedness, and syncope
may cause by slow heart rate, Adams-
Stokes Syndrome may occurs in sever case.
First heart sound varies in intensity, will
appear booming first sound
FIRST DEGREE A-V HEART
BLOCK
Rate: variable
P wave: normal
QRS: normal
Conduction: impulse originates in the SA node but has prolonged
conduction in the AV junction; P-R interval is > 0.20 seconds.
Rhythm: regular
This is the most common conduction disturbance. It occurs in both
healthy and diseased hearts.
First degree AV block can be due to:
inferior MI,
digitalis toxicity
hyperkalemia
increased vagal tone
acute rheumatic fever
myocarditis.
Interventions include treating the underlying cause and observing for
progression to a more advanced AV block.
SECOND DEGREE A-V BLOCK
MOBITZ TYPE I (WENCKEBACK)
Rate: variable
P wave: normal morphology with constant P-P interval
QRS: normal
Conduction: the P-R interval is progressively longer until one P
wave is blocked; the cycle begins again following the blocked P
wave.
Rhythm: irregular
Second degree AV block type I occurs in the AV node above the
Bundle of His.
It is often transient and may be due to acute inferior MI or digitalis
toxicity.
Treatment is usually not indicated as this rhythm usually produces
no symptoms.
SECOND DEGREE A-V BLOCK
MOBITZ TYPE II
Rate: variable
P wave: normal with constant P-P intervals
QRS: usually widened because this is usually associated with a
bundle branch block.
Conduction: P-R interval may be normal or prolonged, but it is
constant until one P wave is not conducted to the ventricles.
Rhythm: usually regular when AV conduction ratios are constant
This block usually occurs below the Bundle of His and may
progress into a higher degree block.
It can occur after an acute anterior MI due to damage in the
bifurcation or the bundle branches.
It is more serious than the type I block.
Treatment is usually artificial pacing.
THIRD DEGREE (COMPLETE)
A-V

BLOCK
Rate: atrial rate is usually normal; ventricular rate is usually less than 70/bpm.
The atrial rate is always faster than the ventricular rate.
P wave: normal with constant P-P intervals, but not "married" to the QRS
complexes.
QRS: may be normal or widened depending on where the escape pacemaker
is located in the conduction system
Conduction: atrial and ventricular activities are unrelated due to the complete
blocking of the atrial impulses to the ventricles.
Rhythm: irregular
Complete block of the atrial impulses occurs at the A-V junction, common
bundle or bilateral bundle branches.
Another pacemaker distal to the block takes over in order to activate the
ventricles or ventricular standstill will occur.
May be caused by:
digitalis toxicity
acute infection
MI and
degeneration of the conductive tissue.
Treatment modalities include:
external pacing and atropine for acute, symptomatic episodes and
permanent pacing for chronic complete heart block.
AV Block
Treatment:
1. I or II degree AV block neednt
antibradycardia agent therapy
2. II degree II type and III degree
AV block need antibradycardia
agent therapy
3. Implant Pace Maker
Intraventricular Block
Intraventricular conduction
system:
1. Right bundle branch
2. Left bundle branch
3. Left anterior fascicular
4. Left posterior fascicular
Intraventricular Block
Etiology:
Myocarditis, valve disease,
cardiomyopathy, CAD, hypertension,
pulmonary heart disease, drug
toxicity, Lenegre disease, Levs
disease et al.
Manifestation:
Single fascicular or bifascicular block
is asymptom; tri-fascicular block may
have dizziness; palpitation, syncope
and Adams-stokes syndrome
 Intraventricular

Block
Therapy:
1. Treat underlying disease
2. If the patient is asymptom; no
treat,
3. bifascicular block and incomplete
trifascicular block may progress to
complete block, may need implant
pace maker if the patient with
syncope
RIGHT BUNDLE BRANCH
BLOCK
Rate: variable
P wave: normal if the underlying rhythm is sinus
QRS: wide; > 0.12 seconds
Conduction: This block occurs in the right or left bundle branches
or in both. The ventricle that is supplied by the blocked bundle is
depolarized abnormally.
Rhythm: regular or irregular depending on the underlying rhythm.
Left bundle branch block is more ominous than right bundle
branch block because it usually is present in diseased hearts. Both
may be caused by hypertension, MI, or cardiomyopathy. A
bifasicular block may progress to third degree heart block.
Treatment is artificial pacing for a bifasicular block that is
associated with an acute MI.
PVC BIGEMNY
Rate: variable
P wave: usually obscured by the QRS, PST or T wave of the PVC
QRS: wide > 0.12 seconds; morphology is bizarre with the ST segment and the T wave
opposite in polarity. May be multifocal and exhibit different morphologies.
Conduction: the impulse originates below the branching portion of the Bundle of His;
full compensatory pause is characteristic.
Rhythm: irregular. PVC's may occur in singles, couplets or triplets; or in bigeminy,
trigeminy or quadrigeminy.

PVCs can occur in healthy hearts. For example, an increase in circulating

catecholamines can cause PVCs. They also occur in diseased hearts and from
drug (such as digitalis) toxicities.
Treatment is required if they are:
associated with an acute MI,
occur as couplets, bigeminy or trigeminy,
are multifocal, or
are frequent (>6/min).
Interventions include:
lidocaine,
pronestyl, or
quinidine.
VENTRICULAR
TACHYCARDIA
Rate: usually between 100 to 220/bpm, but can be as rapid as 250/bpm
P wave: obscured if present and are unrelated to the QRS complexes.
QRS: wide and bizarre morphology
Conduction: as with PVCs
Rhythm: three or more ventricular beats in a row; may be regular or irregular.
Ventricular tachycardia almost always occurs in diseased hearts.
Some common causes are:
CAD
acute MI
digitalis toxicity
CHF
ventricular aneurysms.
Patients are often symptomatic with this dysrhythmia.
Ventricular tachycardia can quickly deteriorate into ventricular fibrillation.
Electrical countershock is the intervention of choice if the patient is
symptomatic and rapidly deteriorating.
Some pharmacological interventions include lidocaine, pronestyl, and
bretylium.
TORSADE DE POINTES
Rate: usually between 150 to 220/bpm,
P wave: obscured if present
QRS: wide and bizarre morphology
Conduction: as with PVCs
Rhythm: Irregular
Paroxysmal starting and stopping suddenly
Hallmark of this rhythm is the upward and downward deflection of the QRS
complexes around the baseline. The term Torsade de Pointes means "twisting about
the points."
Consider it V-tach if it doesnt respond to antiarrythmic therapy or treatments
Caused by:
drugs which lengthen the QT interval such as quinidine
electrolyte imbalances, particularly hypokalemia
myocardial ischemia
Treatment:
Synchronized cardioversion is indicated when the patient is unstable.
IV magnesium
IV Potassium to correct an electrolyte imbalance
Overdrive pacing
VENTRICULAR
FIBRILLATION
Rate: unattainable
P wave: may be present, but obscured by ventricular waves
QRS: not apparent
Conduction: chaotic electrical activity
Rhythm: chaotic electrical activity
This dysrhythmia results in the absence of cardiac output.
Almost always occurs with serious heart disease, especially acute
MI.
The course of treatment for ventricular fibrillation includes:
immediate defibrillation and ACLS protocols.
Identification and treatment of the underlying cause is also needed.
 IDIOVENTRICULAR RHYTHM
Rate: 20 to 40 beats per minute
P wave: Absent
QRS: Widened
Conduction: Failure of primary pacemaker
Rhythm: Regular
Absent P wave
Widened QRS > 0.12 sec.
Also called " dying heart" rhythm
Pacemaker will most likely be needed to re-establish a normal heart rate.
Causes:
Myocardial Infarction
Pacemaker Failure
Metabolic imbalance
Myoardial Ischemia
Treatment goals include measures to improve cardiac output and establish a normal
rhythm and rate.
Options include:
Atropine
Pacing
Caution: Supressing the ventricular rhythm is contraindicated because that rhythm
protects the heart from complete standstill.
VENTRICULAR STANDSTILL
(ASYSTOLE)
Rate: none
P wave: may be seen, but there is no ventricular response
QRS: none
Conduction: none
Rhythm: none
Asystole occurs most commonly following the termination of
atrial, AV junctional or ventricular tachycardias. This pause is
usually insignificant.
Asystole of longer duration in the presence of acute MI and CAD
is frequently fatal.
Interventions include:
CPR,
artificial pacing, and
atropine.
 Recognizing and Naming Beats & Rhythms

QRS is slightly different but still narrow,

Atrial Escape Beat indicating that conduction through the
ventricle is relatively normal
normal ("sinus") beats

sinus node doesn't fire leading

to a period of asystole (sick
sinus syndrome)
p-wave has different shape
indicating it did not originate in
the sinus node, but somewhere
in the atria. It is therefore called
an "atrial" beat
 Recognizing and Naming Beats & Rhythms

Junctional Escape Beat

QRS is slightly different but still narrow,
indicating that conduction through the
ventricle is relatively normal

there is no p wave, indicating that it did

not originate anywhere in the atria, but
since the QRS complex is still thin and
normal looking, we can conclude that the
beat originated somewhere near the AV
junction. The beat is therefore called a
"junctional" or a nodal beat
 Recognizing and Naming Beats & Rhythms

QRS is wide and much different ("bizarre") looking

than the normal beats. This indicates that the beat
originated somewhere in the ventricles and
Ventricular
consequently, conduction through the ventricles did
Escape Beat
not take place through normal pathways. It is
therefore called a ventricular beat

there is no p wave, indicating that the beat

did not originate anywhere in the atria
actually a "retrograde p-wave may sometimes be
seen on the right hand side of beats that
originate in the ventricles, indicating that
depolarization has spread back up through the
atria from the ventricles
 Recognizing and Naming Beats & Rhythms

Ectopic Beats or Rhythms

beats or rhythms that originate in places other than the SA node
the ectopic focus may cause single beats or take over and pace
the heart, dictating its entire rhythm
they may or may not be dangerous depending on how they affect
the cardiac output

Causes of Ectopic Beats or Rhythms

hypoxic myocardium - chronic pulmonary disease, pulmonary embolus
ischemic myocardium - acute MI, expanding MI, angina
sympathetic stimulation - nervousness, exercise, CHF, hyperthyroidism
drugs & electrolyte imbalances - antiarrhythmic drugs, hypokalemia,
imbalances of calcium and magnesium
bradycardia - a slow HR predisposes one to arrhythmias
enlargement of the atria or ventricles producing stretch in pacemaker cells
The Re-Entry Mechanism of Ectopic Beats & Rhythms

Electrical Impulse

Cardiac
Conduction
Tissue

Fast Conduction Path Slow Conduction Path

Slow Recovery Fast Recovery

Tissues with these type of circuits may exist:

in microscopic size in the SA node, AV node, or any type of heart tissue
in a macroscopic structure such as an accessory pathway in WPW
The Re-Entry Mechanism of Ectopic Beats & Rhythms

Premature Beat Impulse

Cardiac
Conduction
Repolarizing Tissue
Tissue
(long refractory period)

Fast Conduction Path Slow Conduction Path

Slow Recovery Fast Recovery

1. An arrhythmia is triggered by a premature beat

2. The beat cannot gain entry into the fast conducting
pathway because of its long refractory period and
therefore travels down the slow conducting pathway only
The Re-Entry Mechanism of Ectopic Beats & Rhythms

Cardiac
Conduction
Tissue

Fast Conduction Path Slow Conduction Path

Slow Recovery Fast Recovery

3. The wave of excitation from the premature beat

arrives at the distal end of the fast conducting
pathway, which has now recovered and therefore
travels retrogradely (backwards) up the fast
pathway
The Re-Entry Mechanism of Ectopic Beats & Rhythms

Cardiac
Conduction
Tissue

Fast Conduction Path Slow Conduction Path

Slow Recovery Fast Recovery

4. On arriving at the top of the fast pathway it finds the

slow pathway has recovered and therefore the wave of
excitation re-enters the pathway and continues in a
circular movement. This creates the re-entry circuit
 Re-entry Circuits as Ectopic Foci and Arrhythmia Generators

Atrio-Ventricular Nodal Re-entry

supraventricular tachycardia
Atrial Re-entry Ventricular Re-entry
atrial tachycardia ventricular tachycardia
atrial fibrillation
atrial flutter

Atrio-Ventricular Re-entry
Wolf Parkinson White
supraventricular tachycardia
 Recognizing and Naming Beats & Rhythms

Clinical Manifestations of Arrhythmias

many go unnoticed and produce no symptoms

palpitations ranging from noticing or being aware of ones heart

beat to a sensation of the heart beating out of the chest
if Q is affected (HR > 300) lightheadedness and syncope, fainting

drugs & electrolyte imbalances - antiarrhythmic drugs, hypokalemia,

imbalances of calcium and magnesium
very rapid arrhythmias u myocardial oxygen demand r ischemia
and angina
sudden death especially in the case of an acute MI
 Recognizing and Naming Beats & Rhythms

Premature Ventricular Contractions (PVCs, VPBs, extrasystoles):

A ventricular ectopic focus discharges causing an early beat
Ectopic beat has no P-wave (maybe retrograde), and QRS complex is "wide and bizarre"
QRS is wide because the spread of depolarization through the ventricles is abnormal (aberrant)
In most cases, the heart circulates no blood (no pulse because of an irregular squeezing motion
PVCs are sometimes described by lay people as skipped heart beats

R on T
phenom em on

M u lt if o c a l C o m p e n s a to ry p a u s e
P V C 's a fte r th e o c c u r a n c e o f a P V C
 Recognizing and Naming Beats & Rhythms
Characteristics of PVC's
PVCs dont have P-waves unless they are retrograde (may be buried in T-Wave)
T-waves for PVCs are usually large and opposite in polarity to terminal QRS
Wide (> .16 sec) notched PVCs may indicate a dilated hypokinetic left ventricle
Every other beat being a PVC (bigeminy) may indicate coronary artery disease
Some PVCs come between 2 normal sinus beats and are called interpolated PVCs

The classic PVC note the

compensatory pause Interpolated PVC note the sinus
rhythm is undisturbed
 Recognizing and Naming Beats & Rhythms

PVC's are Dangerous When:

They are frequent (> 30% of complexes) or are increasing in frequency
The come close to or on top of a preceding T-wave (R on T)
Three or more PVC's in a row (run of V-tach)
Any PVC in the setting of an acute MI
PVC's come from different foci ("multifocal" or "multiformed")

These dangerous phenomenon may preclude the occurrence of deadly arrhythmias:

Ventricular Tachycardia
Ventricular Fibrillation The sooner defibrillation takes place,
the increased likelihood of survival

R on T phenomenon

time

Unconverted V-tach r V-fib

sinus beats V-tach
 Recognizing and Naming Beats & Rhythms

Notes on V-tach:
Causes of V-tach
Prior MI, CAD, dilated cardiomyopathy, or it may be idiopathic (no known cause)
Typical V-tach patient
MI with complications & extensive necrosis, EF<40%, d wall motion, v-aneurysm)
V-tach complexes are likely to be similar and the rhythm regular
Irregular V-Tach rhythms may be due to to:
breakthrough of atrial conduction
atria may capture the entire beat beat
an atrial beat may merge with an ectopic ventricular beat (fusion beat)

Fusion beat - note p- Capture beat - note that

wave in front of PVC and the complex is narrow
the PVC is narrower than enough to suggest normal
the other PVCs this ventricular conduction.
indicates the beat is a This indicates that an
product of both the sinus atrial impulse has made it
node and an ectopic through and conduction
ventricular focus through the ventricles is
relatively normal.
 Recognizing and Naming Beats & Rhythms

Premature Atrial Contractions (PACs):

An ectopic focus in the atria discharges causing an early beat
The P-wave of the PAC will not look like a normal sinus P-wave (different morphology)
QRS is narrow and normal looking because ventricular depolarization is normal
PACs may not activate the myocardium if it is still refractory (non-conducted PACs)
PACs may be benign: caused by stress, alcohol, caffeine, and tobacco
PACs may also be caused by ischemia, acute MIs, d electrolytes, atrial hypertrophy
PACs may also precede PSVT

Non conducted PAC Non conducted PAC

PAC
distorting a T-wave
 Recognizing and Naming Beats & Rhythms

Premature Junctional Contractions (PJCs):

An ectopic focus in or around the AV junction discharges causing an early beat
The beat has no P-wave
QRS is narrow and normal looking because ventricular depolarization is normal
PJCs are usually benign and require not treatment unless they initiate a more serious rhythm

PJC
 Recognizing and Naming Beats & Rhythms

Atrial Fibrillation (A-Fib):

Multiple ectopic reentrant focuses fire in the atria causing a chaotic baseline
The rhythm is irregular and rapid (approx. 140 150 beats per minute)
Q is usually d by 10% to 20% (no atrial kick to ventricular filling)
May be seen in CAD (especially following surgery), mitral valve stenosis, LV hypertrophy, CHF
Treatment: DC cardioversion & O2 if patient is unstable
drugs: (rate control) & Ca++ channel blockers, digitalis, to d AV Conduction
amiodarone to d AV conduction + prolong myocardial AP (u refractoriness of myocardium)
The danger of thromboembolic events are enhanced due to d flow in left atrial appendage
Treatment: anticoagulant drugs (Warfarin / Coumadin)
International Normalized Ratio (INR normalized PT time) should be between 2 and 3.
 Recognizing and Naming Beats & Rhythms

Atrial Flutter:
A single ectopic macroreentrant focuses fire in the atria causing the fluttering baseline
AV node cannot transmit all impulses (atrial rate: 250 350 per minute)
ventricular rhythm may be regular or irregular and range from 150 170 beats / minute
Q may d, especially at high ventricular rates
A-fib and A-flutter rhythm may alternate these rhythms may also alternate with SVTs
May be seen in CAD (especially following surgery), VHD, history of hypertension, LVH, CHF
Treatment: DC cardioversion if patient is unstable
drugs: (goal: rate control) Ca++ channel blockers to d AV conduction
amiodarone to d AV conduction + prolong myocardial AP (u refractoriness of myocardium)
The danger of thromboembolic events is also high in A-flutter
 Recognizing and Naming Beats & Rhythms

Multifocal Atrial Tachycardia (MAT):

Multiple ectopic focuses fire in the atria, all of which are conducted normally to the ventricles
QRS complexes are almost identical to the sinus beats
Rate is usually between 100 and 200 beats per minute
The rhythm is always IRREGULAR
P-waves of different morphologies (shapes) may be seen if the rhythm is slow
If the rate < 100 bpm, the rhythm may be referred to as wandering pacemaker
Commonly seen in pulmonary disease, acute cardiorespiratory problems, and CHF
Treatments: Ca++ channel blockers, blockers, potassium, magnesium, supportive therapy for
underlying causes mentioned above (antiarrhythmic drugs are often ineffective)

Note different P-wave Note IRREGULAR

morphologies when the rhythm in the tachycardia
tachycardia begins
 Recognizing and Naming Beats & Rhythms

Paroxysmal (of sudden onset) Supraventricular Tachycardia (PSVT) :

A single reentrant ectopic focuses fires in and around the AV node, all of which are conducted
normally to the ventricles (usually initiated by a PAC)
QRS complexes are almost identical to the sinus beats
Rate is usually between 150 and 250 beats per minute
The rhythm is always REGULAR
Possible symptoms: palpitations, angina, anxiety, polyuruia, syncope (d Q)
Prolonged runs of PSVT may result in atrial fibrillation or atrial flutter
May be terminated by carotid massage
u carotid pressure r u baroreceptor firing rate r u vagal tone r d AV conduction
Treatment: ablation of focus, Adenosine (d AV conduction), Ca++ Channel blockers

Note REGULAR rhythm

Rhythm usually begins in the tachycardia
with PAC
ECG ARTIFACT
Artifact occurs when something causes a
disruption in monitoring.

Some common causes are:

AC interference -causes 60 cycle artifact
Muscle tremors
Respiratory artifact-wandering baseline
Loose electrode
Broken lead wire
Cardioversion
Synchronized shock with the QRS
complex
PSVT
TREAT UNDERLYING CAUSE
DRUGS: ADENOSINE, -BLOCKERS,
DIGOXIN, MS, QUINIDINE
CAROTID / VAGAL MANEUVERS
SYNCHRONIZED CARDIOVERSION IF
UNSTABLE
Ventricular Arrhythmias

ORIGINATES IN VENTRICLES
PATIENT MAY BE SYMPTOMATIC,
REQUIRES IMMEDIATE ATTENTION
PVC, couplet, bigeminy, trigeminy
V-TACH (ventricular tachycardia)
V-Fib (Ventricular fibrillation)
PREMATURE VENTRICULAR CONTRACTION
(PVC)
EARLY IRREGULAR VENTRICULAR BEATS
QRS IS WIDE /BIZZARE
CAN BE CHRONIC ASYMPTOMATIC
ABNORMALITY OR WARNING OF SERIOUS
DYSRHYTHMIA
PREMATURE VENTRICULAR CONTRACTION
(PVC)
ETIOLOGY:
HYPOXIA
DIGOXIN TOXICITY
MECHANICAL STIMULATION
ELECTROLYTE (K) IMBALANCE
MI
PVCs
PREMATURE VENTRICULAR CONTRACTION
(PVC)
CLINICAL SIGNS:
DEPEND ON FREQUENCY
PVC SHORT DIASTOLIC FILLING TIME
C.O.
FREQUENT PVC SENSATION OF
PALPATIONS, SKIPPED BEATS
BIGEMINY PVC EVERY OTHER BEAT
TRIGEMINY PVC EVERY 3RD BEAT
PREMATURE VENTRICULAR CONTRACTION
(PVC)

TREATMENT:
TREAT IMPAIRED HEMODYNAMICS
ANTIARRHYTHMICS
OXYGEN
MONITOR FOR PVC LANDING ON
T-WAVE
OBSERVE FOR UNIFOCAL (VS) MULTIFOCAL
Ventricular Arrhythmias
VENTRICULAR TACHYCARDIA
3 OR MORE PVCs
QRS IS WIDE/ BIZARRE

EXTREMELY SERIOUS
MAY LEAD TO LETHAL RHYTHMS

ETIOLOGY: SAME CAUSES AS PVC,

ALSO CARDIOMYOPATHY,
MYOCARDIAL IRRITABILITY
Ventricular Tachycardia
Treatment
VT /W PULSE - CARDIOVERT
MONITOR MORE CLOSELY
PREPARE FOR CARDIOVERSION
(O2, LIDOCAINE, TREAT CAUSE)
VT W/O PULSE - DEFIBRILLATE
VENTRICULAR FIBRILLATION
TOTAL UNORGANIZED MULTIFOCAL
RHYTHM, VENTRICLES QUIVER,
NO CARDIAC OUTPUT
V-fib
ETIOLOGY:
SAME AS VT, PVC
SURGICAL MANIPULATION OF HEART
FAILED CARDIOVERSION
CLINICAL SIGNS:
SAME AS CARDIAC ARREST
EKG SHOWS DISORGANIZED
RHYTHM
V-fib
TREATMENT
IMMEDIATE DEFIBRILLATION X3
CPR
SURVIVAL IS < 10% FOR EVERY
MINUTE THE PATIENT REMAINS IN
V-fib
SCREAM for Vfib and
Pulseless VTach
1.Shock360J* monophasic, 1st and
subsequent shocks.(Shock every 2 minutes
if indicated)
2.CPR After shock, immediately begin chest
compressions followed by respirations (30:2
ratio) for 2 minutes.
3.Rhythm check after 2 minutes of CPR (and
after every 2 minutes of CPR thereafter)
and shock again if indicated. Check pulse
only if an organized or non-shockable
rhythm is present.
SCREAM
CARDIAC ARREST
VENTRICULAR ASYSTOLE
80 90% DUE TO V-fib
TOTAL ABSENCE OF ELECTRICAL AND
MECHANICAL ACTIVITY
ETIOLOGY
TRAUMA
OVERDOSE
MI
CLINICAL SIGNS
ASYSTOLE or V-fib
NO DEFINABLE WAVE FORMS
ABSENCE OF VITAL SIGNS
Ventricular Asystole

Acronym Comments
T Transcutaneous Only effective with early
Pacemaker implementaion
E Epinephrine 1 mg IV q3-5 min
A Atropine 1 mg IV q3-5 min
PEA- Pulseless Electrical
Activity
Asystole Algorithm
PEA
Problem search
Epinephrine 1mg IV/IO q3-5min
Atropine- with a slow HR, I mg IV/IO q3-
5min
Consider termination of efforts if asystole
persists despite appropriate interventions.
CARDIAC ARREST
Review ACLS Guidelines
TREATMENT: IMMEDIATE CPR
2005
A. AIRWAY/ ADVANCED AIRWAY CONTROL
B. BREATHING/ POSITIVE PRESSURE
VENTILATION
C. CIRCULATION/ CPR, START IV
D. DEFIBRILLATE (V-fib, V-tach ONLY)
E. DRUGS-Antidysrhythmic tx
CARDIAC ARREST
EPINEPHRINE 1:10,000 IV PUSH
REPEAT Q 5 MIN.
AMIODORONE:
ATROPINE:
VASOPRESSIN:
CONSIDER ANTIARRHYTHMICS
USE ACLS ALGORITHMS
CARDIAC ARREST
TREATMENT: POST CARDIAC ARREST
MONITOR -
CARDIAC STATUS
RESPIRATORY STATUS
TREAT UNDERLYING CAUSE
EMOTIONAL SUPPORT
SAFE ENVIRONMENT
 DEFBRILLATION (vs)
CARDIOVERSION
DEFIBRILLATION
ASYNCHRONOUS ELECTRICAL DISCHARGE
THAT CAUSES DEPOLARIZATION OF ALL
MYOCARDIAL CELLS AT ONCE.
THIS ALLOWS (HOPEFULLY) THE SA NODE TO
RESTORE ITS PACEMAKER FUNCTION AND
DICTATE A REGULAR SINUS RHYTHM.
USED FOR PULSELESS V-tach AND V-fib
VOLTAGE: 200 360 joules (stacked shock)
or AED
CARDIOVERSION (aka)
SYNCHRONIZED
CONVERSION
ELECTRICAL IMPULSE IS DISCHARGED
DURING QRS (VENTRICULAR
DEPOLARIZATION)
USUALLY TIMED /W CARDIAC MONITOR TO
PREVENT SHOCK ON
T-WAVE

USED FOR RAPID A-fib, V-tach /W PULSE AND

PERSISTENT PAT / PSVT

VOLTAGE: 50 100 joules

 EQUIPMENT REVIEW
DEFIBRILLATOR
SELECT ENERGY LEVEL, THEN CHARGE
PADDLES
USE 25 POUNDS OF PRESSURE WHEN APPLIED TO
CHEST, Placed 2nd RICS and 5th LAAS
CONDUCTING AGENT
GEL OR PAD WHICH ESTABLISHES SKIN CONTACT,
REDUCES SKIN BURNS
JOULES
MEASUREMENT OF ELECTRICAL ENERGY
DISCHARGES
NO ONE SHOULD COME IN CONTACT WITH PATIENT
OR BED DURING DISCHARGE
 HEART BLOCK
DEPRESSED CONDUCTION OF IMPULSE
FROM ATRIA TO VENTRICLES
AV NODE BECOMES DEFECTIVE AND
IMPULSES (P-WAVES) ARE BLOCKED FROM
BEING TRANSMITTED TO VENTRICLES
FIRST DEGREE
SECOND DEGREE
TYPE I
TYPE II
THIRD DEGREE
 1 HEART BLOCK

PR INTERVAL > 0.20 SECONDS

CAUSES: MAY BE NORMAL VARIANT
INFERIOR WALL MI
DRUGS: DIGOXIN
VERAPAMIL
TREATMENT:
MONITOR
OBSERVE FOR SYMPTOMS
FIRST DEGREE HEART BLOCK
2 HEART BLOCK

ONE OR MORE P-WAVES ARE NOT

CONDUCTED THROUGH THE VENTRICLE

HEART RATE - VENTRICULAR RATE

SLOW TO NORMAL
ATRIAL RATE MAY BE 2 4 Xs
FASTER THAN VENTRICULAR
2 HEART BLOCK
CAUSES: ORGANIC HEART DISEASE
MI, Dig toxicity, B and Ca Channel Blockers
DIGOXIN TOXICITY
SYMPTOMS
Tx:
Monitor HR
Atropine
Temporary pacemaker
Avoid meds that decrease conductivity
2 TYPES OF 2 HEART BLOCK
MOBITZ TYPE I- Wenkeback
MOBITZ TYPE II
Second Degree Heart Block
Mobitz I
PRI becomes progressively longer until
drops QRS
Second Degree Heart Block
Mobitz Type II
PRI constant and regular, but in a 2:1 ,
3:1 pattern
 3 HEART BLOCK
(COMPLETE HEART BLOCK)
ATRIAL IMPULSES & VENTRICULAR RESPONSE
ARE IN TOTAL DISASSOCIATION
P-WAVES ARE SEEN & ARE IRREGULAR
QRS COMPLEX ARE SEEN & ARE IRREGULAR
(ESCAPE RHYTHM)
NO CORRELATION BETWEEN P-WAVES & QRS
(RATE IS SLOW) independent rhythms
3 HEART BLOCK
(COMPLETE HEART BLOCK)
CAUSES
ORGANIC HEART DISEASE
MI
DRUGS
ELECTROLYTE IMBALANCE
EXCESS VAGAL TONE
SIGNS & SYMPTOMS
EXTREME DIZZINESS
HYPOTENSION
SYNCOPE
S/S OF C.O.
ALTERED MENTAL STATUS
NSR vs 3 RD
Degree Block
3 HEART BLOCK
(COMPLETE HEART BLOCK)
TREATMENT
PACEMAKER
TEMPORARY
OR
PERMANENT
PACEMAKER
Indications: Speed up a slow HR or Slow down
a rapid HR
ELECTRICAL DEVICE THAT DELIVERS
CONTROLLED ELECTRICAL STIMULUS
THROUGH ELECTRODES PLACED IN CONTACT
WITH HEART MUSCLE
2 PIECES
PULSE GENERATOR IMPLANTED IN CHEST
WALL UNDER R CLAVICLE
PACEMAKER ELECTRODES IMPLANTED IN
MYOCARDIAL TISSUE
Paced Rhythm
Pacemaker spike
PACEMAKER
TEMPORARY
PACEMAKER
USED IN
EMERGENCY
SITUATION
FIXED
(COMPETITIVE)
PACEMAKER SENDS
STIMULUS TO
VENTRICLE AT A
FIXED RATE,
REGARDLESS OF
VENTRICULAR
ACTIVITY
Types of Pacemakers
Use a 5 letter code
system, first 3 used
more often:
1. Chamber being
paced: A, V, D
2. Chamber being
sensed: A, V, D, O
3. Type of response by
the PM to the
sensing: I, T, D, O
PATIENT TEACHING
Carry PM ID card
MEDI ALERT BRACELET
Avoid swimming, golf and weight lifting
AVOID MRI
Check PM q3-6 mos.
PACEMAKER SURVEILANCE
Monitor pulse rates
Dont hold cell phones over generators
AUTOMATIC IMPLANTABLE
CARDIOVERSION DEFIBRILLATOR
(AICD)
PROVIDES INTERNAL SHOCKS WHEN
SERIOUS ARRHYTHMIA IS DETECTED (V-
tach OR V-fib)
Has a pulse generator and a sensor that
monitors the heart
If pt has dysrhythmia it delivers a shock
which the pt will feel

USEFUL WHEN ARRHYTHMIA IS

UNRESPONSIVE TO MEDS OR SURGICAL
ABLATION OR IRRITABLE MYOCARDIAL
TISSUE
References

http://www.rnceus.com/ekg/ekgsecond2.ht
ml
ACLS Guidelines 2005
www.EMS-ED.net
http://www.doctorshangout.com/forum/topi
cs/acls-algorithms-1