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

formation1. Sinus pulse2. Ectopic pulse3. Triggered activity Abnormal heart pulse

conduction1. Reentry2. Conduct block

Classification of Arrhythmia Abnormal heart pulse formation1. Sinus arrhythmia2. Atrial arrhythmia3. Atrioventricular junctional

arrhythmia4. Ventricular arrhythmia Abnormal heart pulse conduction1. Sinus-atrial block2. Intra-atrial block3. Atrio-ventricular block4. 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 blocker2. II class: ß-receptor blocker3. III class: Potassium channel

blocker4. IV class: Calcium channel blocker5. Others: Adenosine, Digital

Anti-bradycardia agents

1. ß-adrenic receptor activator2. M-cholinergic receptor blocker3. 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 tachyarrhythmia1. 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: ß-receptor blocker1. Propranolol: Non-selective2. Metoprolol: Selective ß1-

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 ß-blocker effect Bretylium

Anti-tachycardia agents: IV class: be used in

supraventricular tachycardia1. Verapamil2. 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, coffee2. 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 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, 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 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 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 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 > 3s3. Type II SAB4. Nonsinus tachyarrhythmia ( SVT, AF

or Af).5. SNRT > 1530ms, SNRTc > 525ms6. Instinct heart rate < 80bmp

Sick Sinus Syndrome (SSS) Therapy:1. Treat the etiology2. 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: 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:1. Atrial rate is around 100-200bpm;2. Warmup phenomena3. 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: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 cases5. 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 disease2. 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

patients2. Etiology just like atrial flutter3. 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 disease2. 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.

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 AVNRT1. 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 AVRT1.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 AVRT1. 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 arrhythmia

Ventricular Premature Contractions (VPCs) Etiology:1. Occur in normal person2. Myocarditis, CAD, valve heart

disease, hyperthyroidism, Drug toxicity (digoxin, quinidine and anti-anxiety drug)

3. electrolyte disturbance, anxiety, drinking, coffee

VPCs

Manifestation: 1. palpitation2. dizziness3. 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 diseas2. ß-blocker, amiodarone3. 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

tone2. 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 disease2. 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 degree1. Type I: prolong the conductive

time2. Type II: partial block3. 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 block2. Second-degree AV block: further

subdivided into type I and type II3. 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 needn’ t

antibradycardia agent therapy2. 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 branch2. Left bundle branch3. Left anterior fascicular4. Left posterior fascicular

Intraventricular Block 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

Intraventricular Block

Therapy:1. Treat underlying disease2. 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 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" rhythmPacemaker 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 BeatQRS 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 PathSlow Recovery

Slow Conduction PathFast 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



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



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



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 ultifoca l P V C 's

C om pensa to ry pausea fte r the occu rance o f a P V C

R on T phenom em on


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 beatsUnconverted 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

PACNon 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 ATTENTIONPVC, couplet, bigeminy, trigeminyV-TACH (ventricular tachycardia)V-Fib (Ventricular fibrillation)

PREMATURE VENTRICULAR CONTRACTION(PVC)

EARLY IRREGULAR VENTRICULAR BEATSQRS IS WIDE /BIZZARECAN BE CHRONIC ASYMPTOMATIC

ABNORMALITY OR WARNING OF SERIOUS DYSRHYTHMIA


ETIOLOGY:

HYPOXIA

DIGOXIN TOXICITY

MECHANICAL STIMULATION

ELECTROLYTE (K) IMBALANCE

MI


CLINICAL SIGNS:DEPEND ON FREQUENCYPVC SHORT DIASTOLIC FILLING TIME

C.O.FREQUENT PVC – SENSATION OF

PALPATIONS, SKIPPED BEATSBIGEMINY – PVC EVERY OTHER BEATTRIGEMINY – PVC EVERY 3RD BEAT


TREATMENT:TREAT IMPAIRED HEMODYNAMICSANTIARRHYTHMICSOXYGENMONITOR FOR PVC LANDING ON

T-WAVEOBSERVE FOR UNIFOCAL (VS) MULTIFOCAL

Ventricular Arrhythmias

VENTRICULAR TACHYCARDIA3 OR MORE PVC’sQRS 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 - CARDIOVERTMONITOR MORE CLOSELYPREPARE FOR CARDIOVERSION

(O2, LIDOCAINE, TREAT CAUSE)

VT W/O PULSE - DEFIBRILLATE

VENTRICULAR FIBRILLATIONTOTAL UNORGANIZED MULTIFOCAL

RHYTHM, VENTRICLES QUIVER,

NO CARDIAC OUTPUT

V-fib

ETIOLOGY: SAME AS VT, PVCSURGICAL MANIPULATION OF HEARTFAILED CARDIOVERSION

CLINICAL SIGNS:SAME AS CARDIAC ARRESTEKG 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 VTach1.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

ETIOLOGYTRAUMAOVERDOSEMI

CLINICAL SIGNS

ASYSTOLE or V-fibNO DEFINABLE WAVE FORMSABSENCE 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 ARRESTReview 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

DEFIBRILLATIONASYNCHRONOUS 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-fibVOLTAGE: 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 ONT-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 AGENTGEL OR PAD WHICH ESTABLISHES SKIN CONTACT, REDUCES SKIN BURNS

JOULESMEASUREMENT OF ELECTRICAL ENERGY

DISCHARGESNO 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 MIDRUGS: DIGOXIN

VERAPAMIL TREATMENT:

MONITOROBSERVE 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 X’s

FASTER THAN VENTRICULAR

2° HEART BLOCKCAUSES: ORGANIC HEART DISEASE

MI, Dig toxicity, B and Ca Channel Blockers

DIGOXIN TOXICITYSYMPTOMS Tx:

Monitor HR Atropine Temporary pacemaker

Avoid meds that decrease conductivity2 TYPES OF 2° HEART BLOCK

MOBITZ TYPE I- Wenkeback

MOBITZ TYPE II

Second Degree Heart BlockMobitz I PRI becomes progressively longer until

drops QRS

Second Degree Heart BlockMobitz 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 DISEASEMIDRUGSELECTROLYTE IMBALANCEEXCESS VAGAL TONE

SIGNS & SYMPTOMS EXTREME DIZZINESS HYPOTENSION SYNCOPE S/S OF C.O. ALTERED MENTAL STATUS

NSR vs 3RD 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 PIECESPULSE GENERATOR IMPLANTED IN CHEST WALL UNDER R CLAVICLEPACEMAKER ELECTRODES IMPLANTED IN MYOCARDIAL TISSUE

Paced Rhythm

Pacemaker spike

PACEMAKER TEMPORARY

PACEMAKERUSED 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/

topics/acls-algorithms-1

Arrhythmia

Health & Medicine

Transcript of Arrhythmia