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A trifasicular block is a physiological mechanism... the " third degree block " is

what is found on the EKG.

A description of trifascicular block is found below my comments.

A third degree block could be caused by medications (most often digoxin

toxicity), a trifascicular block, a complete AV note dysfunction or a block in

the fibers between the bifurcation of the left/right bundles (infranodal) and AV

node. I am not sure if there are any other causes besides these.

In regards to atropine... in 3rd degree block, narrow QRS complexes indicate

that the bundles are probably not blocked and atropine may be effective for

restarting the AV node or bypassing the upper block.. If a patient started off

with a bifascicular block for example, which could be a combination of right

bundle (the RBBB) and left anterior (negative leads II, III, aVF) or less

commonly the posterior (negative lead I) fascicle, or both left fascicles (not

as a LBBB but as noted previously) and had a transient block of the remaining

fascicle/bundle then it is more serious and atropine will be ineffective.

This is something that I learned not too long ago myself but I do find it

intriguing!

AHA says atropine is a IIa recommendation see:

http://www.acc.org/clinical/guidelines/nov96/1999/jac1716pIIIa.htm#atropine

BTW, lidocaine is strongly relatively contraindicated in bifascicular blocks...

(little known tidbit)

Regards

Nick " I am not a electrophysiologist but I play one on TV " Nudell

ha ha ha

Reference:

(V1-V2), often of the shape rsR, rSR or rR.

3.. Repolarization disturbance in leads V1-V2 (ST segment depression, T wave

inversion).

4.. Wide S waves in left leads I, V5 and V6.

5.. The shape of QRS varies greatly and is dependent on the underlying

disease.

Differential diagnosis

a.. Right ventricular hypertrophy (RVH)

b.. Wolff-Parkinson-White syndrome (WPW)

c.. Peripheral conduction disturbances

Clinical significance

a.. Commonly seen without serious heart disease.

b.. Clinical significance depends on the possible underlying disease, which

may be myocardial infarction, myocarditis, pulmonary embolism, COPD (cor

pulmonale).

c.. Often a sequela of congenital heart disease that remains even after

corrective surgery (ASD).

d.. RBBB appearing in middle age often signifies ischaemic heart disease,

cardiomyopathy, or COPD (= RVH).

e.. In acute anterior infarction and associated LAHB, RBBB is a sign of large

myocardial damage and poor prognosis.

f.. Complicates ECG diagnostics and the judgment of:

a.. posterior infarction

b.. LVH and RVH.

g.. Incomplete RBBB (same shape but duration < 0.12 s) is a common and

innocent ECG change in young endurance athletes. The aetiology of the rSR' in

these cases is not a conduction defect.

LBBB

ECG features

1.. QRS duration at least 0.12 s

2.. M-shaped broad R wave in leads I, aVL, V5-V6 and without Q wave.

3.. ST deviation and T wave directed away from the QRS complex (repolarization

disturbance).

4.. Broad and deep S shaped rS or QS in leads V1-V2

5.. Variations in shape depend on simultaneous LVH, infarction etc. The axis

is often to the left.

Differential diagnosis

a.. WPW

b.. Peripheral conduction disturbances

Clinical significance

a.. Frequently a sign of heart disease.

b.. LBBB at middle age usually reflects acquired heart disease, most commonly

LVH, coronary heart disease or myocarditis. The underlying disease determines

the prognosis. Occasionally no underlying disease can be diagnosed.

c.. In connection with acute myocardial infarction (AMI), recent LBBB predicts

extensive myocardial damage and poor prognosis.

d.. LBBB complicates or prevents the ECG diagnosis of AMI. Thrombolysis is

indicated in clinical diagnosis of infarction and recent LBBB in ECG.

e.. The sensitivity of the voltage criteria for LBBB decreases, but the

specificity increases. LBBB as such predicts LVH.

f.. Incomplete LBBB (same shape but duration < 0.12 s) is usually caused by

LVH. Exact differentiation from LBBB is not necessary.

LAHB (LAFB), left anterior hemiblock

ECG features

1.. Frontal axis deviation to the left (-30°--90°)

2.. Deep S wave of the shape rS in leads II, III and aVF

3.. qR in leads I and aVL.

4.. Minor widening of QRS (< 0.12 s).

5.. Repolarization disturbance absent

a.. Additional criteria that support the diagnosis are regression of the R

wave and a deep S wave in left chest leads.

Differential diagnosis

a.. LVH (left axis deviation)

b.. Anterior infarction (R regression)

Clinical significance

a.. LAHB is the most common intraventricular block. The left anterior branch

is easily damaged and a block does not mean that the damage to the heart is

considerable.

b.. LAHB complicates ECG diagnostics in many ways, also when computer programs

are used, which is why the physician should be familiar with it.

c.. In young patients without risk factors, LAHB is a benign and innocent ECG

abnormality without marked clinical significance.

d.. At middle age, LAHB predicts heart disease, which is not necessarily

severe.

LPHB (LPFB), left posterior hemiblock

ECG features

a.. Axis to the right

b.. QRS complexes to opposite directions compared with LAHB

Clinical significance

a.. Extremely rare.

b.. Usually associated with massive posterior infarction.

c.. Differential diagnosis: RVH

Bifascicular blocks

RBBB+LAHB

a.. The most common block.

b.. ECG features are the same as in RBBB. In addition, frontal axis deviation

to the left (-30°--90°): rS in leads II, III and aVF.

Clinical significance

a.. In asymptomatic patients the prognosis is frequently good. In myocardial

diseases the condition may progress to a trifascicular block.

b.. In myocardial infarction this is a sign of extensive myocardial damage and

predicts total AV block.

c.. A pacemaker often necessary if the condition is associated with AMI. When

a long PQ time is associated with the conduction disturbance, the condition is

called trifascicular block (see later), which is always an indication for a

pacemaker.

Trifascicular blocks: RBBB+LAHB+AV block

a.. A bifascicular block with grade I or II AV block. The condition is more

severe if the PQ time is long, suggesting a defect in the bundle of His. Caution

with drugs that prolong PQ time is necessary.

b.. The most common type is RBBB + LAHB + prolonged PQ time.

c.. The risk of total AV block is high, which is why pacemaker is often

necessary. The prognosis is rather poor even with a pacemaker.

--------------------------------------------------------------------------------

Author: Markku Ellonen

Article ID: ebm00050 (004.003)

© 2003 The Finnish Medical Society Duodecim

--------------------------------------------------------------------------------\

----------------------

Atropine:

By its parasympatholytic (anticholinergic) activity, atropine sulfate reduces

vagal tone, enhances the rate of discharge of the sinus node, and facilitates AV

conduction.75 It may be given as an adjunct to morphine administration when

nausea and vomiting occur. During the early moments to hours of acute ischemia

or acute MI, atropine is particularly useful in treating sinus bradycardia

associated with reduced cardiac output and signs of peripheral hypoperfusion,

including arterial hypotension, confusion, faintness, or frequent premature

ventricular complexes.76 In this setting, leg elevation and intravenous

administration of atropine may be lifesaving.

Atropine for Atrioventricular Block, Sinus Bradycardia, or Ventricular Asystole

Atropine is the drug of choice for the occasional treatment of type I

second-degree AV block, especially when complicating inferior MI. It is

occasionally useful in third-degree AV block at the AV node level in either

restoring AV conduction or enhancing the junctional response. When AV block or

sinus bradycardia is associated with CHF, hypotension, or frequent and complex

ventricular arrhythmias, atropine may improve AV conduction, increase the sinus

rate, and avoid the need for immediate insertion of a transvenous pacemaker.77

As a rule, however, in the absence of hemodynamic compromise, treatment of sinus

bradycardia or first- or second-degree AV block is not indicated. Similarly,

atropine is rarely, if ever, the drug of choice for management of type II

second-degree AV block. On occasion, while failing to improve AV block, atropine

may increase the sinus rate, and, in fact, enhance the block.

The recommended dosage of atropine for bradycardia is 0.5 to 1.0 mg

intravenously (IV), repeated if needed every 3 to 5 minutes to a total dose of

no more than 2.5 mg (0.03 to 0.04 mg/kg), the amount that produces complete

vagal blockade. Atropine may also be therapeutic in ventricular asystole, for

which the recommended dose is 1 mg IV, to be repeated every 3 to 5 minutes

(while CPR continues) if asystole persists. The total cumulative dose should not

exceed 2.5 mg over 2.5 hours. The peak action of atropine given intravenously is

observed within 3 minutes.1

Side Effects

When administered in doses of less than 0.5 mg or other than intravenously,

atropine may produce a paradoxic effect (namely, bradycardia and depression of

AV conduction),78 which is due either to central reflex stimulation of the vagus

or a peripheral parasympathomimetic effect on the heart. Urinary retention is

not uncommon following administration of atropine and can be deleterious to the

patient with acute MI. Repeated administration of atropine may produce adverse

central nervous system effects, including hallucinations and fever. Careful

dosing and observation after administration of atropine is necessary because the

sinus tachycardia that follows may increase ischemia. Rarely, ventricular

tachycardia and fibrillation occur after intravenous administration of

atropine.79

Pacing is the treatment of choice for symptomatic bradycardia not responding

promptly to atropine administration.

Re: Paramedic KSAs (Knowledge, Skills, Abilities)

Just a side note Gene...not sure if this is where you were going with your

thought... but if the students cannot answer it in this frame, then they

just 'don't know'. I find that most people who take ACLS do not know this,

as the only education on these meds occurs during the ACLS lectures and AHA

says it should not be a 'regular' part of the algo, since you should start

with pacing...

Atropine in 3rd degree block is relatively indicated. If the patient has a

'trifasicular block' that is new for example or AV node dysfunction, it is

possible that the atropine will enhance the AV nodal conduction and/or a

bypass tract that will get sinus pacing past the block.

If needed, I will search for a reference for this point, don't have it at

the tip of my fingers.

Regards

Nick

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Gene

I know its probably a trade secret but I would really like to learn more about

your approach! I also have the attitude that a fun class will be more beneficial

then a boring or scary class...

Please feel free to email me offlist if you would prefer!

Thanks

Nick

____________________________________________

Nick Nudell, NREMT-P, CCEMT-P

California

nudell@...

" Perception is reality " - Wise Old Paramedic

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If there are only three fascicles (left anterior bundle, left posterior

bundle, and right bundle) between the atria and ventricles, and all three

are blocked, it is a third degree AV block. You are saying it seems that

there is a " third degree AB block " and " trifasicular block " and these are

separate entities? That is not what I learned in medical school and

residency. Please provide reference for your claims. Your response below is

muble-jumble. Provide the references if something is stated as fact.

Re: Paramedic KSAs (Knowledge, Skills, Abilities)

A trifasicular block is a physiological mechanism... the " third degree

block " is what is found on the EKG.

A description of trifascicular block is found below my comments.

A third degree block could be caused by medications (most often digoxin

toxicity), a trifascicular block, a complete AV note dysfunction or a block

in the fibers between the bifurcation of the left/right bundles (infranodal)

and AV node. I am not sure if there are any other causes besides these.

In regards to atropine... in 3rd degree block, narrow QRS complexes indicate

that the bundles are probably not blocked and atropine may be effective for

restarting the AV node or bypassing the upper block.. If a patient started

off with a bifascicular block for example, which could be a combination of

right bundle (the RBBB) and left anterior (negative leads II, III, aVF) or

less commonly the posterior (negative lead I) fascicle, or both left

fascicles (not as a LBBB but as noted previously) and had a transient block

of the remaining fascicle/bundle then it is more serious and atropine will

be ineffective.

This is something that I learned not too long ago myself but I do find it

intriguing!

AHA says atropine is a IIa recommendation see:

http://www.acc.org/clinical/guidelines/nov96/1999/jac1716pIIIa.htm#atropine

BTW, lidocaine is strongly relatively contraindicated in bifascicular

blocks... (little known tidbit)

Regards

Nick " I am not a electrophysiologist but I play one on TV " Nudell

ha ha ha

Reference:

(V1-V2), often of the shape rsR, rSR or rR.

3.. Repolarization disturbance in leads V1-V2 (ST segment depression, T

wave inversion).

4.. Wide S waves in left leads I, V5 and V6.

5.. The shape of QRS varies greatly and is dependent on the underlying

disease.

Differential diagnosis

a.. Right ventricular hypertrophy (RVH)

b.. Wolff-Parkinson-White syndrome (WPW)

c.. Peripheral conduction disturbances

Clinical significance

a.. Commonly seen without serious heart disease.

b.. Clinical significance depends on the possible underlying disease,

which may be myocardial infarction, myocarditis, pulmonary embolism, COPD

(cor pulmonale).

c.. Often a sequela of congenital heart disease that remains even after

corrective surgery (ASD).

d.. RBBB appearing in middle age often signifies ischaemic heart disease,

cardiomyopathy, or COPD (= RVH).

e.. In acute anterior infarction and associated LAHB, RBBB is a sign of

large myocardial damage and poor prognosis.

f.. Complicates ECG diagnostics and the judgment of:

a.. posterior infarction

b.. LVH and RVH.

g.. Incomplete RBBB (same shape but duration < 0.12 s) is a common and

innocent ECG change in young endurance athletes. The aetiology of the rSR'

in these cases is not a conduction defect.

LBBB

ECG features

1.. QRS duration at least 0.12 s

2.. M-shaped broad R wave in leads I, aVL, V5-V6 and without Q wave.

3.. ST deviation and T wave directed away from the QRS complex

(repolarization disturbance).

4.. Broad and deep S shaped rS or QS in leads V1-V2

5.. Variations in shape depend on simultaneous LVH, infarction etc. The

axis is often to the left.

Differential diagnosis

a.. WPW

b.. Peripheral conduction disturbances

Clinical significance

a.. Frequently a sign of heart disease.

b.. LBBB at middle age usually reflects acquired heart disease, most

commonly LVH, coronary heart disease or myocarditis. The underlying disease

determines the prognosis. Occasionally no underlying disease can be

diagnosed.

c.. In connection with acute myocardial infarction (AMI), recent LBBB

predicts extensive myocardial damage and poor prognosis.

d.. LBBB complicates or prevents the ECG diagnosis of AMI. Thrombolysis is

indicated in clinical diagnosis of infarction and recent LBBB in ECG.

e.. The sensitivity of the voltage criteria for LBBB decreases, but the

specificity increases. LBBB as such predicts LVH.

f.. Incomplete LBBB (same shape but duration < 0.12 s) is usually caused

by LVH. Exact differentiation from LBBB is not necessary.

LAHB (LAFB), left anterior hemiblock

ECG features

1.. Frontal axis deviation to the left (-30°--90°)

2.. Deep S wave of the shape rS in leads II, III and aVF

3.. qR in leads I and aVL.

4.. Minor widening of QRS (< 0.12 s).

5.. Repolarization disturbance absent

a.. Additional criteria that support the diagnosis are regression of the R

wave and a deep S wave in left chest leads.

Differential diagnosis

a.. LVH (left axis deviation)

b.. Anterior infarction (R regression)

Clinical significance

a.. LAHB is the most common intraventricular block. The left anterior

branch is easily damaged and a block does not mean that the damage to the

heart is considerable.

b.. LAHB complicates ECG diagnostics in many ways, also when computer

programs are used, which is why the physician should be familiar with it.

c.. In young patients without risk factors, LAHB is a benign and innocent

ECG abnormality without marked clinical significance.

d.. At middle age, LAHB predicts heart disease, which is not necessarily

severe.

LPHB (LPFB), left posterior hemiblock

ECG features

a.. Axis to the right

b.. QRS complexes to opposite directions compared with LAHB

Clinical significance

a.. Extremely rare.

b.. Usually associated with massive posterior infarction.

c.. Differential diagnosis: RVH

Bifascicular blocks

RBBB+LAHB

a.. The most common block.

b.. ECG features are the same as in RBBB. In addition, frontal axis

deviation to the left (-30°--90°): rS in leads II, III and aVF.

Clinical significance

a.. In asymptomatic patients the prognosis is frequently good. In

myocardial diseases the condition may progress to a trifascicular block.

b.. In myocardial infarction this is a sign of extensive myocardial damage

and predicts total AV block.

c.. A pacemaker often necessary if the condition is associated with AMI.

When a long PQ time is associated with the conduction disturbance, the

condition is called trifascicular block (see later), which is always an

indication for a pacemaker.

Trifascicular blocks: RBBB+LAHB+AV block

a.. A bifascicular block with grade I or II AV block. The condition is

more severe if the PQ time is long, suggesting a defect in the bundle of

His. Caution with drugs that prolong PQ time is necessary.

b.. The most common type is RBBB + LAHB + prolonged PQ time.

c.. The risk of total AV block is high, which is why pacemaker is often

necessary. The prognosis is rather poor even with a pacemaker.

----------------------------------------------------------------------------

----

Author: Markku Ellonen

Article ID: ebm00050 (004.003)

© 2003 The Finnish Medical Society Duodecim

----------------------------------------------------------------------------

--------------------------

Atropine:

By its parasympatholytic (anticholinergic) activity, atropine sulfate

reduces vagal tone, enhances the rate of discharge of the sinus node, and

facilitates AV conduction.75 It may be given as an adjunct to morphine

administration when nausea and vomiting occur. During the early moments to

hours of acute ischemia or acute MI, atropine is particularly useful in

treating sinus bradycardia associated with reduced cardiac output and signs

of peripheral hypoperfusion, including arterial hypotension, confusion,

faintness, or frequent premature ventricular complexes.76 In this setting,

leg elevation and intravenous administration of atropine may be lifesaving.

Atropine for Atrioventricular Block, Sinus Bradycardia, or Ventricular

Asystole

Atropine is the drug of choice for the occasional treatment of type I

second-degree AV block, especially when complicating inferior MI. It is

occasionally useful in third-degree AV block at the AV node level in either

restoring AV conduction or enhancing the junctional response. When AV block

or sinus bradycardia is associated with CHF, hypotension, or frequent and

complex ventricular arrhythmias, atropine may improve AV conduction,

increase the sinus rate, and avoid the need for immediate insertion of a

transvenous pacemaker.77 As a rule, however, in the absence of hemodynamic

compromise, treatment of sinus bradycardia or first- or second-degree AV

block is not indicated. Similarly, atropine is rarely, if ever, the drug of

choice for management of type II second-degree AV block. On occasion, while

failing to improve AV block, atropine may increase the sinus rate, and, in

fact, enhance the block.

The recommended dosage of atropine for bradycardia is 0.5 to 1.0 mg

intravenously (IV), repeated if needed every 3 to 5 minutes to a total dose

of no more than 2.5 mg (0.03 to 0.04 mg/kg), the amount that produces

complete vagal blockade. Atropine may also be therapeutic in ventricular

asystole, for which the recommended dose is 1 mg IV, to be repeated every 3

to 5 minutes (while CPR continues) if asystole persists. The total

cumulative dose should not exceed 2.5 mg over 2.5 hours. The peak action of

atropine given intravenously is observed within 3 minutes.1

Side Effects

When administered in doses of less than 0.5 mg or other than intravenously,

atropine may produce a paradoxic effect (namely, bradycardia and depression

of AV conduction),78 which is due either to central reflex stimulation of

the vagus or a peripheral parasympathomimetic effect on the heart. Urinary

retention is not uncommon following administration of atropine and can be

deleterious to the patient with acute MI. Repeated administration of

atropine may produce adverse central nervous system effects, including

hallucinations and fever. Careful dosing and observation after

administration of atropine is necessary because the sinus tachycardia that

follows may increase ischemia. Rarely, ventricular tachycardia and

fibrillation occur after intravenous administration of atropine.79

Pacing is the treatment of choice for symptomatic bradycardia not responding

promptly to atropine administration.

Re: Paramedic KSAs (Knowledge, Skills, Abilities)

Just a side note Gene...not sure if this is where you were going with your

thought... but if the students cannot answer it in this frame, then they

just 'don't know'. I find that most people who take ACLS do not know this,

as the only education on these meds occurs during the ACLS lectures and

AHA

says it should not be a 'regular' part of the algo, since you should start

with pacing...

Atropine in 3rd degree block is relatively indicated. If the patient has a

'trifasicular block' that is new for example or AV node dysfunction, it is

possible that the atropine will enhance the AV nodal conduction and/or a

bypass tract that will get sinus pacing past the block.

If needed, I will search for a reference for this point, don't have it at

the tip of my fingers.

Regards

Nick

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Gene,

There soon will be a national instructor's course, if the NAEMSEs has

its say. They have developed and tested a broad based instructor's course

that is being released or is in the process of being released. The contents

can be accessed at their website at www.naemse.org. This looks to be an

excellent program.

Jeanne E. Amis, RN, LP

Education Director

Marfa City/County EMS

Re: Paramedic KSAs (Knowledge, Skills, Abilities)

> In a message dated 11/7/2003 12:59:42 AM Central Standard Time,

> mreed_911@... writes:

>

> > Define " quality instructor. " Name one body that accredits, nationally,

> > paramedic educators, programs or courses. A rhetorical question, but

one

> > you're free to elaborate on.

> >

>

> Nobody accredits instructors nationally. The state certifications are for

> having been through a 40 hour adult learning seminar that will qualify the

> applicant for instructor status.

>

> I know what a quality instructor is, and so do most of you.

>

> A quality instructor is first of all, honest to a fault. S/he tells it

like

> it is not matter what. S/he will not lie or bend the truth to get

students to

> join the program.

>

> A quality instructor will know, backwards, forwards, and sideways, the

> materials that he's teaching. That means understanding the

pathophysiology of all

> conditions that you'll be teaching, and all the standard treatments, drugs

and

> what their characteristics are, and critical thinking about situations

that

> you're likely to be encountered.

>

>

>

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