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V. Taylor
“Disease in any of
these or the
ventricular
myocardium can
cause abnormalities
of heart rate or
incoordination of
cardiac contraction.”
Causes of arrhythmias
Ischaemia
(MI or CAD)
Electrolyte
disturbances
Clinical features of arrhythmias:
Palpitation, Chest pain, Presyncope/ Syncope, Hypotension, Pulmonary oedema
LV aneurysm
Mitral valve
disease
Cardiomyopathy
Pericarditis
Myocarditis
Abberant
conduction
pathways
Alcohol
Caffeine
Drugs
Pneumonia
Smoking
www.styletax.com
Clinical classification of arrhythmias
• Heart rate (increased/ decreased)
• Heart rhythm (regular/ irregular)
• Site of origin (supraventricular/
ventricular)
• Complexes on ECG (narrow/ broad)
Arrhythmias are often due to:
Re-entry or Abnormal Automaticity or Heart Block
Re-Entry
www.cvphysiology.com/Arrhythmias/A008c.htm
Requires:
• An area of unidirectional block (e.g.
accessory pathway) / slow conducting tissue
• Time taken to propagate impulse around ring
of tissue must exceed refractory period.
 So slowing of conduction (e.g.
myocardial damage) favours re-entry.
Leads to continuous circulation of the
impulse, known as a circus movement.
Abnormal Automaticity
Arrhythmias are often due to:
Re-entry or Abnormal Automaticity or Heart Block
When pacemaker activity arises in parts of the heart
other than the SAN.
Predisposing factors: Catecholamine action
Partial depolarisation
Catecholamines act on β1 adrenoceptors to increase
rate of depolarisation during phase 4 causing normally
quiescent parts to spontaneously depolarise.
Partial depolarisation can result from ischaemic damage and is probably
due to the decrease ATP produced under conditions of decrease oxygen
supply causing decreased activity of the Na pump.
www.cvphysiology.com
Arrhythmias are often due to:
Re-entry or Abnormal Automaticity or Heart Block
Heart block
• Results from ischaemic damage
or fibrosis of conducting system
(most commonly AVN).
Conducting System
• SAN block
• AVN block
• Bundle branch block
• Hemiblock
www.mc.vanderbilt.edu
Arrhythmias
Tachyarrhythmia
(>100bpm)
Heart Block
SAN
block
AVN
block
Intraventricular
block
1st
degree 2nd
degree
3rd
degree
RBBB LBBB
Narrow Complex
(QRS<120msec)
Broad Complex
(QRS>120msec)
VT Ventricular
ectopics
SVT/ AF with
abnormal
conduction
Sinus
tachy
SVT AFAtrial
flutter
Regular Irregular VF
Hemiblock
Abnormal sinus rhythm
Heart rate is controlled by input from the autonomic nervous system:
• Increased sympathetic activity  tachycardia (>100bpm)
(Sinus tachycardia)
• Increased parasympathetic input  bradycardia (<50bpm)
(Sinus bradycardia)
Other factors affecting sinus rhythm include: caffeine, alcohol
Sinus Rhythm is the regular rhythm set by the sinoatrial node
Narrow Complex Tachycardias
1. Supraventricular tachcardia (SVT)
• Regular rhythm
• Heartbeat not controlled by the SA node
• Another part of the heart overrides this timer with faster impulses.
• ‘Trigger' is somewhere above the ventricles & spreads to the ventricles.
For example:
S&S: HR 140-200bpm, dizziness, palpitations, SOB, angina, BP drop.
• A small area in one of the atria may become more 'excitable' than usual and start
to produce electrical impulses.
• A 'short circuit' in the electrical pathways of the heart may develop. This can
make electrical impulses go round and round this section of the heart.
Three of the most common supraventricular tachycardias are:
• atrial tachycardia
• atrioventricular reentrant tachycardia (AVRN)
• atrioventricular nodal reentrant tachycardia (AVNRT)
www.ambulancetechnicianstudy.co.uk
2. Atrial Fibrillation (AF)
Narrow Complex Tachycardias
ECG:
• No P wave
• Irregular QRS complexes
• Chaotic, irregular rhythm
• Atria depolarise at 300-600bpm, with the
AVN responding intermittently
Paroxysmal: self-terminating
Persistent: can be converted to sinus rhythm
Permanent: unable to maintain sinus rhythm
• Common in the elderly (nearly 10%)
• Main risk is embolic stroke
• Causes: HF, hypertension, ischaemia, MI, mitral
valve disease, pneumonia, alcohol, thyroid
www.cardionetics.comwww.londoncardiac.ca
3. Atrial Flutter
Narrow Complex Tachycardias
• A rapid and regular atrial contractions
(usually 120 to 350 times/minute)
ECG :
Classic ‘saw-tooth’ appearance
• Not all atrial contractions are necessarily
conducted to the ventricles due to a
variable block within the AVN.
• Can unmask flutter waves by carotid
sinus massage or IV adenosine
(transiently block AVN)
www.cardionetics.comwww.londoncardiac.ca
Broad Complex Tachycardias
1. Ventricular Tachycardia
• Occurs when a rapid and repetitive conduction path
exists entirely within the ventricles.
• The rhythm may stabilise, extinguish and revert to
sinus rhythm, or degenerate into ventricular fibrillation
2. Ventricular Fibrillation
With ventricular fibrillation, collapse and sudden cardiac death will soon
follow unless medical intervention is swiftly provided.
www.cardionetics.com
Broad complex tachycardias can also be caused by SVT or AF with abnormal
conduction or pre-excitation.
Broad Complex Tachycardias
3. Ventricular Ectopics
• Over half the population have silent, or
asymptomatic, ventricular ectopics.
• The most common type of ventricular ectopic beat is
premature, causing ventricular contraction before the
underlying rhythm would normally depolarise the ventricles.
Patterns:
•Bigeminy (every other beat)
•Trigeminy (every third beat)
•Quadrigeminy (every fourth beat)
•Couplets or triplets
•Salvos (four to seven)
•Episodes (eight or more)
E.g. Bigeminy
• Every other beat is a ventricular ectopic.
• These are premature, wider, and larger
than the sinus beats.
www.cardionetics.com
Heart Block
1st
Degree Heart Block
2nd
Degree Heart Block
Mobitz Type I (Wenkebach)
ECG:
PR interval >0.2 secs
(one small box)
• There is a delay in conduction through the AVN.
• Does not require treatment.
• The AVN conducts each successive
impulse earlier and earlier
• Eventually, an impulse arrives when the
node is not able to conduct it.
Eventually, an impulse arrives when the node is not able to conduct it.
ECG:
Not all P waves followed by QRS
www.cardionetics.comwww.co.livingston.mi.us
Heart Block
2nd Degree Heart Block
Mobitz Type II
• Not every atrial depolarisation is
conducted to the ventricles
Block can be:
• Constant
 2:1 (every other
impulse is
conducted)
 3:1 (every third
impulse is
conducted)
• Periodic (dropped
beats occur without
any pattern)
Mobitz type II may progress to…
www.cardionetics.com
3rd
Degree Heart Block (Complete heart block)
Heart Block
• Complete interruption of the conduction from the atria to the ventricles
• The QRS complexes are caused by slower, automatic escape rhythms
The atria are contracting at 59 bpm (grey circles)
The ventricles are contracting at 38 bpm (red arrows)
ECG:
Regular RR interval
No correlation
between P & QRS
Stokes-Adams attacks:
A transient arrhythmia causing decreased cardiac output & loss of consciousness.
Recovery is in seconds.
www.cardionetics.com
Heart Block
Bundle Branch Block
There should be a QS or rS complex
in lead V1 & a monophasic R wave
in leads I & V6.
There should be a terminal R wave in
lead V1 (e.g., R, rR', rsR', rSR' or qR')
& a slurred S wave in leads I & V6.
RBBB LBBB
• BBB leads to a delay in the depolarisation of part of the ventricular muscle
en.wikipedia.org
 Class I: Block sodium channels.
 Ia (quinidine, procainamide,
disopyramide)
 Ib (lignocaine)
 Ic (flecainide)
 Class II: ß-adrenoceptor
antagonists (atenolol, sotalol)
 Class III: Block K+ channels.
Delays phase 3 repolarization
and increases the ERP
(suppress re-entrant rhythms)
(amiodarone, sotalol)
 Class IV: Calcium channel
antagonists. Impair impulse
propagation in nodal and
damaged areas (verapamil)
Treatment: Medical (quick reminder)
www.cvphysiology.com
Treatment: Pacing
• First implanted in humans in 1958…
now 20,000/ year
• Supply electrical stimulation to
myocardial contraction
• Last 7- 15 years
Pacemakers use electrical impulses, delivered by electrodes
contacting the heart muscles, to regulate the beating of the heart.
The pacemaker lead is inserted into a
vein located in the upper chest.
It is placed in the right atrium or the
right ventricle with the visual guidance
of x-rays.
www.hgcardio.com
Treatment: Pacing
Indications for a pacemaker:
Temporary: Symptomatic bradycardia, After acute MI if complete AV
block, Mobitz type I or II, Suppressing drug-resistant tachyarrhythmias.
Permanent: Complete AV block, Mobitz type II, Persistent AV block after
anterior MI, Symptomatic bradycardia, Drug-resistant tachyarrhythmias
Types of pacemaker: look for the 3 letter code (VVI most common in UK)
1st
letter =
chamber paced
• A = atrial
• V = ventricular
• D = dual (A+V)
2nd
letter =
chamber sensed
• A = atrial
• V = ventricular
• D = dual (A+V)
• 0 = none
1st
letter = pacemaker
response
• T = triggered
• I = inhibited
• D = dual (T+I)
• R = reverse
www.matadorrecords.com

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Arrhythmias

  • 2. “Disease in any of these or the ventricular myocardium can cause abnormalities of heart rate or incoordination of cardiac contraction.”
  • 3. Causes of arrhythmias Ischaemia (MI or CAD) Electrolyte disturbances Clinical features of arrhythmias: Palpitation, Chest pain, Presyncope/ Syncope, Hypotension, Pulmonary oedema LV aneurysm Mitral valve disease Cardiomyopathy Pericarditis Myocarditis Abberant conduction pathways Alcohol Caffeine Drugs Pneumonia Smoking www.styletax.com
  • 4. Clinical classification of arrhythmias • Heart rate (increased/ decreased) • Heart rhythm (regular/ irregular) • Site of origin (supraventricular/ ventricular) • Complexes on ECG (narrow/ broad)
  • 5. Arrhythmias are often due to: Re-entry or Abnormal Automaticity or Heart Block Re-Entry www.cvphysiology.com/Arrhythmias/A008c.htm Requires: • An area of unidirectional block (e.g. accessory pathway) / slow conducting tissue • Time taken to propagate impulse around ring of tissue must exceed refractory period.  So slowing of conduction (e.g. myocardial damage) favours re-entry. Leads to continuous circulation of the impulse, known as a circus movement.
  • 6. Abnormal Automaticity Arrhythmias are often due to: Re-entry or Abnormal Automaticity or Heart Block When pacemaker activity arises in parts of the heart other than the SAN. Predisposing factors: Catecholamine action Partial depolarisation Catecholamines act on β1 adrenoceptors to increase rate of depolarisation during phase 4 causing normally quiescent parts to spontaneously depolarise. Partial depolarisation can result from ischaemic damage and is probably due to the decrease ATP produced under conditions of decrease oxygen supply causing decreased activity of the Na pump. www.cvphysiology.com
  • 7. Arrhythmias are often due to: Re-entry or Abnormal Automaticity or Heart Block Heart block • Results from ischaemic damage or fibrosis of conducting system (most commonly AVN). Conducting System • SAN block • AVN block • Bundle branch block • Hemiblock www.mc.vanderbilt.edu
  • 8. Arrhythmias Tachyarrhythmia (>100bpm) Heart Block SAN block AVN block Intraventricular block 1st degree 2nd degree 3rd degree RBBB LBBB Narrow Complex (QRS<120msec) Broad Complex (QRS>120msec) VT Ventricular ectopics SVT/ AF with abnormal conduction Sinus tachy SVT AFAtrial flutter Regular Irregular VF Hemiblock
  • 9. Abnormal sinus rhythm Heart rate is controlled by input from the autonomic nervous system: • Increased sympathetic activity  tachycardia (>100bpm) (Sinus tachycardia) • Increased parasympathetic input  bradycardia (<50bpm) (Sinus bradycardia) Other factors affecting sinus rhythm include: caffeine, alcohol Sinus Rhythm is the regular rhythm set by the sinoatrial node
  • 10. Narrow Complex Tachycardias 1. Supraventricular tachcardia (SVT) • Regular rhythm • Heartbeat not controlled by the SA node • Another part of the heart overrides this timer with faster impulses. • ‘Trigger' is somewhere above the ventricles & spreads to the ventricles. For example: S&S: HR 140-200bpm, dizziness, palpitations, SOB, angina, BP drop. • A small area in one of the atria may become more 'excitable' than usual and start to produce electrical impulses. • A 'short circuit' in the electrical pathways of the heart may develop. This can make electrical impulses go round and round this section of the heart. Three of the most common supraventricular tachycardias are: • atrial tachycardia • atrioventricular reentrant tachycardia (AVRN) • atrioventricular nodal reentrant tachycardia (AVNRT) www.ambulancetechnicianstudy.co.uk
  • 11. 2. Atrial Fibrillation (AF) Narrow Complex Tachycardias ECG: • No P wave • Irregular QRS complexes • Chaotic, irregular rhythm • Atria depolarise at 300-600bpm, with the AVN responding intermittently Paroxysmal: self-terminating Persistent: can be converted to sinus rhythm Permanent: unable to maintain sinus rhythm • Common in the elderly (nearly 10%) • Main risk is embolic stroke • Causes: HF, hypertension, ischaemia, MI, mitral valve disease, pneumonia, alcohol, thyroid www.cardionetics.comwww.londoncardiac.ca
  • 12. 3. Atrial Flutter Narrow Complex Tachycardias • A rapid and regular atrial contractions (usually 120 to 350 times/minute) ECG : Classic ‘saw-tooth’ appearance • Not all atrial contractions are necessarily conducted to the ventricles due to a variable block within the AVN. • Can unmask flutter waves by carotid sinus massage or IV adenosine (transiently block AVN) www.cardionetics.comwww.londoncardiac.ca
  • 13. Broad Complex Tachycardias 1. Ventricular Tachycardia • Occurs when a rapid and repetitive conduction path exists entirely within the ventricles. • The rhythm may stabilise, extinguish and revert to sinus rhythm, or degenerate into ventricular fibrillation 2. Ventricular Fibrillation With ventricular fibrillation, collapse and sudden cardiac death will soon follow unless medical intervention is swiftly provided. www.cardionetics.com
  • 14. Broad complex tachycardias can also be caused by SVT or AF with abnormal conduction or pre-excitation. Broad Complex Tachycardias 3. Ventricular Ectopics • Over half the population have silent, or asymptomatic, ventricular ectopics. • The most common type of ventricular ectopic beat is premature, causing ventricular contraction before the underlying rhythm would normally depolarise the ventricles. Patterns: •Bigeminy (every other beat) •Trigeminy (every third beat) •Quadrigeminy (every fourth beat) •Couplets or triplets •Salvos (four to seven) •Episodes (eight or more) E.g. Bigeminy • Every other beat is a ventricular ectopic. • These are premature, wider, and larger than the sinus beats. www.cardionetics.com
  • 15. Heart Block 1st Degree Heart Block 2nd Degree Heart Block Mobitz Type I (Wenkebach) ECG: PR interval >0.2 secs (one small box) • There is a delay in conduction through the AVN. • Does not require treatment. • The AVN conducts each successive impulse earlier and earlier • Eventually, an impulse arrives when the node is not able to conduct it. Eventually, an impulse arrives when the node is not able to conduct it. ECG: Not all P waves followed by QRS www.cardionetics.comwww.co.livingston.mi.us
  • 16. Heart Block 2nd Degree Heart Block Mobitz Type II • Not every atrial depolarisation is conducted to the ventricles Block can be: • Constant  2:1 (every other impulse is conducted)  3:1 (every third impulse is conducted) • Periodic (dropped beats occur without any pattern) Mobitz type II may progress to… www.cardionetics.com
  • 17. 3rd Degree Heart Block (Complete heart block) Heart Block • Complete interruption of the conduction from the atria to the ventricles • The QRS complexes are caused by slower, automatic escape rhythms The atria are contracting at 59 bpm (grey circles) The ventricles are contracting at 38 bpm (red arrows) ECG: Regular RR interval No correlation between P & QRS Stokes-Adams attacks: A transient arrhythmia causing decreased cardiac output & loss of consciousness. Recovery is in seconds. www.cardionetics.com
  • 18. Heart Block Bundle Branch Block There should be a QS or rS complex in lead V1 & a monophasic R wave in leads I & V6. There should be a terminal R wave in lead V1 (e.g., R, rR', rsR', rSR' or qR') & a slurred S wave in leads I & V6. RBBB LBBB • BBB leads to a delay in the depolarisation of part of the ventricular muscle en.wikipedia.org
  • 19.  Class I: Block sodium channels.  Ia (quinidine, procainamide, disopyramide)  Ib (lignocaine)  Ic (flecainide)  Class II: ß-adrenoceptor antagonists (atenolol, sotalol)  Class III: Block K+ channels. Delays phase 3 repolarization and increases the ERP (suppress re-entrant rhythms) (amiodarone, sotalol)  Class IV: Calcium channel antagonists. Impair impulse propagation in nodal and damaged areas (verapamil) Treatment: Medical (quick reminder) www.cvphysiology.com
  • 20. Treatment: Pacing • First implanted in humans in 1958… now 20,000/ year • Supply electrical stimulation to myocardial contraction • Last 7- 15 years Pacemakers use electrical impulses, delivered by electrodes contacting the heart muscles, to regulate the beating of the heart. The pacemaker lead is inserted into a vein located in the upper chest. It is placed in the right atrium or the right ventricle with the visual guidance of x-rays. www.hgcardio.com
  • 21. Treatment: Pacing Indications for a pacemaker: Temporary: Symptomatic bradycardia, After acute MI if complete AV block, Mobitz type I or II, Suppressing drug-resistant tachyarrhythmias. Permanent: Complete AV block, Mobitz type II, Persistent AV block after anterior MI, Symptomatic bradycardia, Drug-resistant tachyarrhythmias Types of pacemaker: look for the 3 letter code (VVI most common in UK) 1st letter = chamber paced • A = atrial • V = ventricular • D = dual (A+V) 2nd letter = chamber sensed • A = atrial • V = ventricular • D = dual (A+V) • 0 = none 1st letter = pacemaker response • T = triggered • I = inhibited • D = dual (T+I) • R = reverse www.matadorrecords.com