Arrhythmia

 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: ß-receptor blocker
3. III class: Potassium channel blocker
4. IV class: Calcium channel blocker
5. Others: Adenosine, Digital

Anti-bradycardia agents
1. ß-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

 Ib class: Perfect to ventricular
tachyarrhythmia
1. Lidocaine
2. Mexiletine

 Ic class: Can be used in ventricular and/or
supra-ventricular tachycardia and
extrasystole.
1. Moricizine
2. Propafenone

 II class: ß-receptor blocker
1. Propranolol: Non-selective
2. Metoprolol: Selective ß1-receptor blocker,
Perfect to hypertension and coronary
artery disease patients associated with
tachyarrhythmia.

 III class: Potassium channel blocker,
extend-spectrum anti-arrhythmia agent.
 Amioarone: Perfect to coronary artery
disease and heart failure patients
 Sotalol: Has ß-blocker effect
 Bretylium

 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 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
 Needn’t 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 (ß-
blocker) , Hypothyriodism, CAD or SSS
 Symptoms:
1. Most patients have no symptoms.
2. Severe bradycardia may cause dizziness, fatigue,
palpitation, even syncope.
 Needn’t 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
 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, ß-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
 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
couldn’t 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
 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

 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

 Therapy:
1. Treat the etiology
2. Treat with drugs: anti-bradycardia
agents, the effect of drug therapy is not
good.
3. Artificial cardiac pacing.

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: Needn’t therapy in the patients
without heart disease. Can be treated with ß-
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:
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 can’t 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:
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 can’t 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, ß-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.
 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, ß-block
4. Antithrombotic therapy: Aspirine,
Warfarin

Atrioventricular Junctional
arrhythmia

Atrioventricular junctional premature
contractions
 Etiology and manifestation is like APCs
 Therapy the underlying disease
 Needn’t 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.
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.

 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

 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

 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.

 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 syndrome)
 There are 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 can’t use digoxin and
verapamil.
3. DC shock: WPW with SVT, AF or Afi produce
agina, syncope and hypotension
4. RFCA

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, ß-
blocker and mexiletine to relief the symptom.
 With structure heart disease (CAD, HBP):
1. Treat the underlying diseas
2. ß-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

 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

 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: ß-blockers,
lidocain or amiodarone
4. RFCA, ICD or surgical therapy

Therapy of Special type VT
 Accelerated idioventricular rhythm:
 usually no symptom, needn’t therapy.
 Atropine increased sinus rhythm
 Tdp:
1. Treat underlying disease,
2. Magnesium iv, atropine or isoprenaline, ß-
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
 It’s 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, lev’s 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.
 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.
 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:
 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 needn’t
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

 Etiology:
 Myocarditis, valve disease, cardiomyopathy,
CAD, hypertension, pulmonary heart disease,
drug toxicity, Lenegre disease, Lev’s disease
et al.
 Manifestation:
 Single fascicular or bifascicular block is
asymptom; tri-fascicular block may have
dizziness; palpitation, syncope and Adams-
stokes syndrome

 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
 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 doesn’t 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.

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
QRS is slightly different but still narrow,
indicating that conduction through the
ventricle is relatively normal
Atrial Escape Beat
Recognizing and Naming Beats & Rhythms

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

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
QRS is wide and much different ("bizarre") looking
than the normal beats. This indicates that the beat
originated somewhere in the ventricles and
consequently, conduction through the ventricles did
not take place through normal pathways. It is
therefore called a “ventricular” beat
Ventricular
Escape Beat
there is no p wave, indicating that the beat
did not originate anywhere in the atria

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

Fast Conduction Path
Slow Recovery
Slow Conduction Path
Fast Recovery
The “Re-Entry” Mechanism of Ectopic Beats & Rhythms
Electrical Impulse
Cardiac
Conduction
Tissue
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

Slow Recovery
Fast Recovery
Premature Beat Impulse
Cardiac
Conduction
Tissue
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
Repolarizing Tissue
(long refractory period)

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
Slow Recovery
Fast Recovery
Cardiac
Conduction
Tissue

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
Slow Recovery
Fast Recovery
Cardiac
Conduction
Tissue

Atrial Re-entry
• atrial tachycardia
• atrial fibrillation
• atrial flutter
Atrio-Ventricular Re-entry
• Wolf Parkinson White
• supraventricular tachycardia
Ventricular Re-entry
• ventricular tachycardia
Atrio-Ventricular Nodal Re-entry
• supraventricular tachycardia
Re-entry Circuits as Ectopic Foci and Arrhythmia Generators

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

Premature Ventricular Contractions (PVC’s, VPB’s, 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
• PVC’s are sometimes described by lay people as “skipped heart beats”
M u lt if o c a l
P V C 's
C o m p e n s a t o r y p a u s e
a fte r t h e o c c u r a n c e o f a P V C
R o n T
p h e n o m e m o n

Characteristics of PVC's
• PVC’s don’t have P-waves unless they are retrograde (may be buried in T-Wave)
• T-waves for PVC’s are usually large and opposite in polarity to terminal QRS
• Wide (> .16 sec) notched PVC’s may indicate a dilated hypokinetic left ventricle
• Every other beat being a PVC (bigeminy) may indicate coronary artery disease
• Some PVC’s come between 2 normal sinus beats and are called “interpolated” PVC’s
Interpolated PVC – note the sinus
rhythm is undisturbed
The classic PVC – note the
compensatory pause

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
sinus beats
Unconverted V-tach r V-fib
V-tach
“R on T phenomenon”
time
The sooner defibrillation takes place,
the increased likelihood of survival

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-
wave in front of PVC and
the PVC is narrower than
the other PVC’s – this
indicates the beat is a
product of both the sinus
node and an ectopic
ventricular focus
Capture beat - note that
the complex is narrow
enough to suggest normal
ventricular conduction.
This indicates that an
atrial impulse has made it
through and conduction
through the ventricles is
relatively normal.

Premature Atrial Contractions (PAC’s):
• 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
• PAC’s may not activate the myocardium if it is still refractory (non-conducted PAC’s)
• PAC’s may be benign: caused by stress, alcohol, caffeine, and tobacco
• PAC’s may also be caused by ischemia, acute MI’s, d electrolytes, atrial hypertrophy
• PAC’s may also precede PSVT
PAC
Non conducted PAC Non conducted PAC
distorting a T-wave

Premature Junctional Contractions (PJC’s):
• 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
• PJC’s are usually benign and require not treatment unless they initiate a more serious rhythm
PJC

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.

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 SVT’s
• 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

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 IRREGULAR
rhythm in the tachycardia
Note different P-wave
morphologies when the
tachycardia begins

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
in the tachycardiaRhythm usually begins
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, β-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

(PVC)
 ETIOLOGY:
HYPOXIA
DIGOXIN TOXICITY
MECHANICAL STIMULATION
ELECTROLYTE (K) IMBALANCE
MI

(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

(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 PVC’s
QRS IS WIDE/ BIZARRE
EXTREMELY SERIOUS
MAY LEAD TO LETHAL RHYTHMS
 ETIOLOGY: SAME CAUSES AS PVC,
ALSO CARDIOMYOPATHY,
MYOCARDIAL IRRITABILITY

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.

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
Pacemaker
Only effective with early
implementaion
E Epinephrine 1 mg IV q3-5 min
A Atropine 1 mg IV q3-5 min

PEA- Pulseless Electrical
Activity
 Asystole Algorithm
 P E A
 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
2005TREATMENT: IMMEDIATE CPR
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

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 X’s
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
 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

3° 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
 Don’t 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.html
 ACLS Guidelines 2005
 www.EMS-ED.net
 http://www.doctorshangout.com/forum/topi
cs/acls-algorithms-1

Arrhythmia

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