Guest guest Posted November 7, 2003 Report Share Posted November 7, 2003 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 Quote Link to comment Share on other sites More sharing options...
Guest guest Posted November 8, 2003 Report Share Posted November 8, 2003 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 Quote Link to comment Share on other sites More sharing options...
Guest guest Posted November 8, 2003 Report Share Posted November 8, 2003 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 Quote Link to comment Share on other sites More sharing options...
Guest guest Posted November 8, 2003 Report Share Posted November 8, 2003 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. > > > Quote Link to comment Share on other sites More sharing options...
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