Professional Documents
Culture Documents
Arrhythmia 130722132907 Phpapp02
Arrhythmia 130722132907 Phpapp02
Therapy:
Treat underlying disease; stopping
digoxin, administer potassium,
lidocaine, phenytoin or propranolol.
Not for DC shock
It can disappear spontaneously. If had
good tolerance, not require therapy.
JUNCTIONAL ESCAPE RHYTHM
Rate: 40-60/bpm
P wave: inverted in leads where they are normally upright; this
happens when the atrial depolarization wave moves towards a
negative (-) lead.P waves may occur before, during or after the QRS,
depending on where the pacemaker is located in the AV junction .
QRS: normal
Conduction: P-R interval < .12 seconds if present.
Rhythm: irregular as a result of the escape beats.
The most common cause of this rhythm in healthy individuals is sinus
bradycardia.
It may also be seen in the presence of a high degree or complete AV
block. If the ventricular rate is slow, hemodynamic compromise may
occur.
Treatment depends upon the underlying cause and the baseline
dysrhythmias.
Atropine or a pacemaker may be used to increase
the ventricular rate.
Paroxysmal tachycardia
Most PSVT (paroxysmal supraventricular
tachycardia) is due to reentrant mechanism.
The incidence of PSVT is higher in AVNRT
(atrioventricular node reentry tachycardia) and
AVRT (atioventricular reentry tachycardia), the
most common is AVNRT (90%)
Occur in any age individuals, usually no structure
heart disease.
Paroxysmal tachycardia
Manifestation:
Occur and terminal abruptly.
Palpitation, dizziness, syncope,
angina, heart failure and shock.
The sever degree of the
symptom is related to
ventricular rate, persistent
duration and underlying disease
Paroxysmal tachycardia
ECG characteristic of AVNRT
1. Heart rate is 150-250 bpm, regular
2. QRS complex is often normal, wide QRS
complex is with aberrant conduction
3. Negative P wave in II III aVF, buried into or
following by the QRS complex.
4. AVN jump phenomena
Paroxysmal tachycardia
ECG characteristic of AVRT
1. Heart rate is 150-250 bpm, regular
2. In orthodromic AVRT, the QRS complex
is often normal, wide QRS complex is
with antidromic AVRT
3. Retrograde P’ wave, R-P’>110ms.
Paroxysmal tachycardia
Therapy:
AVNRT & orthodromic AVRT
1. Increase vagal tone: carotid sinus massage,
Valsalva maneuver.if no successful,
2. Drug: verapamil, adrenosine, propafenone
3. DC shock
Antidromic AVRT:
1. Should not use verapamil, digitalis, and
stimulate the vagal nerve.
2. Drug: propafenone, sotalol, amiodarone
RFCA
Pre-excitation syndrome
(W-P-W 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 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
Ventricular tachycardia
Torsades de points (Tdp): A special type of
polymorphic VT,
Etiology:
1. congenital (Long QT),
2. electrolyte disturbance,
3. antiarrhythmia drug proarrhythmia (IA or IC),
4. antianxiety drug,
5. brain disease,
6. bradycardia
Ventricular tachycardia
Accelerated idioventricular rhythm:
1. Related to increase automatic tone
2. Etiology: Often occur in organic heart
disease, especially AMI reperfusion
periods, heart operation, myocarditis,
digitalis toxicity
VT
Manifestation:
1. Nonsustained VT with no symptom
2. Sustained VT : with symptom and
unstable hemodynamic, patient may feel
palpitation, short of breathness,
presyncope, syncope, angina,
hypotension and shock.
VT
ECG characteristics:
1. Monomorphic VT: 100-250 bpm, occur and
terminate abruptly,regular
2. Accelerated idioventricular rhythm: a runs of 3-10
ventricular beats, rate of 60-110 bpm, tachycardia
is a capable of warm up and close down, often seen
AV dissociation, fusion or capture beats
3. Tdp: rotation of the QRS axis around the baseline,
the rate from 160-280 bpm, QT interval prolonged
> 0.5s, marked U wave
Treatment of VT
1. Treat underlying disease
2. Cardioversion: Hemodynamic unstable VT
(hypotension, shock, angina, CHF) or
hemodynamic stable but drug was no
effect
3. Pharmacological therapy: 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.
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 therapy
2. II degree II type and III degree AV block
need antibradycardia agent therapy
3. Implant Pace Maker
Intraventricular Block
Intraventricular conduction system:
1. Right bundle branch
2. Left bundle branch
3. Left anterior fascicular
4. Left posterior fascicular
Intraventricular Block
Etiology:
Myocarditis, valve disease, cardiomyopathy,
CAD, hypertension, pulmonary heart disease,
drug toxicity, Lenegre disease, 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 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.
Electrical Impulse
Cardiac
Conduction
Tissue
Cardiac
Conduction
Repolarizing Tissue
Tissue
(long refractory period)
Cardiac
Conduction
Tissue
Cardiac
Conduction
Tissue
Atrio-Ventricular Re-entry
• Wolf Parkinson White
• supraventricular tachycardia
Recognizing and Naming Beats & Rhythms
R on T
phenom em on
M u lt if o c a l C o m p e n s a to ry p a u s e
P V C 's a fte r th e o c c u r a n c e o f a P V C
Recognizing and Naming Beats & Rhythms
Characteristics of PVC's
• 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
“R on T phenomenon”
time
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)
PJC
Recognizing and Naming Beats & Rhythms
Atrial Flutter:
• A single ectopic macroreentrant focuses fire in the atria causing the “fluttering” baseline
• AV node cannot transmit all impulses (atrial rate: 250 –350 per minute)
• ventricular rhythm may be regular or irregular and range from 150 –170 beats / minute
• Q may d, especially at high ventricular rates
• A-fib and A-flutter rhythm may alternate – these rhythms may also alternate with 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
Recognizing and Naming Beats & Rhythms
ORIGINATES IN VENTRICLES
PATIENT MAY BE SYMPTOMATIC,
REQUIRES IMMEDIATE ATTENTION
PVC, couplet, bigeminy, trigeminy
V-TACH (ventricular tachycardia)
V-Fib (Ventricular fibrillation)
PREMATURE VENTRICULAR CONTRACTION
(PVC)
EARLY IRREGULAR VENTRICULAR BEATS
QRS IS WIDE /BIZZARE
CAN BE CHRONIC ASYMPTOMATIC
ABNORMALITY OR WARNING OF SERIOUS
DYSRHYTHMIA
PREMATURE VENTRICULAR CONTRACTION
(PVC)
ETIOLOGY:
HYPOXIA
DIGOXIN TOXICITY
MECHANICAL STIMULATION
ELECTROLYTE (K) IMBALANCE
MI
PVCs
PREMATURE VENTRICULAR CONTRACTION
(PVC)
CLINICAL SIGNS:
DEPEND ON FREQUENCY
PVC SHORT DIASTOLIC FILLING TIME
C.O.
FREQUENT PVC – SENSATION OF
PALPATIONS, SKIPPED BEATS
BIGEMINY – PVC EVERY OTHER BEAT
TRIGEMINY – PVC EVERY 3RD BEAT
PREMATURE VENTRICULAR CONTRACTION
(PVC)
TREATMENT:
TREAT IMPAIRED HEMODYNAMICS
ANTIARRHYTHMICS
OXYGEN
MONITOR FOR PVC LANDING ON
T-WAVE
OBSERVE FOR UNIFOCAL (VS) MULTIFOCAL
Ventricular Arrhythmias
VENTRICULAR TACHYCARDIA
3 OR MORE PVC’s
QRS IS WIDE/ BIZARRE
EXTREMELY SERIOUS
MAY LEAD TO LETHAL RHYTHMS
Acronym Comments
T Transcutaneous Only effective with early
Pacemaker implementaion
E Epinephrine 1 mg IV q3-5 min
A Atropine 1 mg IV q3-5 min
PEA- Pulseless Electrical
Activity
Asystole Algorithm
PEA
Problem search
Epinephrine – 1mg IV/IO q3-5min
Atropine- with a slow HR, I mg IV/IO q3-
5min
Consider termination of efforts if
asystole persists despite appropriate
interventions.
CARDIAC ARREST
Review ACLS Guidelines
2005
TREATMENT: IMMEDIATE CPR
http://www.rnceus.com/ekg/ekgsecond2.html
ACLS Guidelines 2005
www.EMS-ED.net
http://www.doctorshangout.com/forum/topi
cs/acls-algorithms-1