Arrhythmias - Ipswich-Year2-Med-PBL-Gp-2

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Transcript Arrhythmias - Ipswich-Year2-Med-PBL-Gp-2

Arrhythmias
Rhythms and Arrhythmia
• SA Node
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Normal sinus rhythm
Sinus Bradycardia
Sinus Tachycardia
Sick Sinus Syndrome
• Atria
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Ectopic beats
Fibrillation
Flutter
Supraventricular tachycardia
Rhythms and Arrhythmia
• AV Node
– Reentrant tachycardia
– 1st 2nd 3rd degree blocks
– Bundle branch block
• Ventricles
– Ectopic beats
– Tachycardia
– Preexitation
– Ischemia
Normal Sinus Rhythm
• Normal sequence of conduction, originating in
the sinus node and proceeding to the
ventricles via the AV node and His-Purkinje
system.
• EKG Characteristics: Regular narrow-complex
rhythm
Sinus Tachycardia Aetiologies
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Fever
Hyperthyroidism
Hypovolaemia
Anxiety
Pheochromocytoma
Sepsis
Anaemia
Exposure to stimulants (nicotine, caffeine) or illicit drugs (amphetamines)
Hypotension and shock
Pulmonary embolism
Acute coronary ischemia and myocardial infarction
Heart failure
Chronic pulmonary disease
Hypoxia
http://www.youtube.com/watch?v=zbDtMtJyVtI
Sinus Bradycardia
• Sinus Bradycardia
– HR< 60 bpm
– QRS is narrow and preceded by p wave
– Can be normal in well-conditioned athletes at rest
or children during sleep
– So when is it not normal?
– Is not normal if the sinus rhythm can’t increase
with exercise
Sinus Bradycardia - aetiologies
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Normal aging
15-25% following AMI
Sick sinus syndrome
Hypothyroidism
Hypothermia
Hypokalemia
Situational: micturation, coughing
Drugs: beta-blockers, digoxin, calcium channel blockers,
amiodarone, lithium
http://www.youtube.com/watch?v=Yff9VvNGL5w&feature
=related
Sick Sinus Syndrome
• Aetiology
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Fibrosis
Atheroschlerosis of RC artery
SLE, collagen vasc diseases
Chagas disease - yeay
Injury, heart surgery
Infiltrative diseases
• sarcoid
• amyloid
• Symptoms
– Weakness
– Palpitations
– Syncope
Disorders of the SA Node
• Sinus arrest
• Tachycardia-bradycardia syndrome
– Alternating brady-tachy causing palpitations
• SA exit block
– Normal SA impulse but conduction to atria is
impaired
Atrial Ectopic Beats
• Ectopic P waves look abnormal
• SA node continues regardless in compensatory delay
• SA node timing is reset if premature SA firing caused by
ectopic – non compensatory
Atrial Fibrillation
• Constant conduction within the atria, multiple circuits,
loss of contractility
• Can be paroxysmal, persistent or permanent
• 1 in 5 strokes caused by AF: patients require
anticoagulation therapy to prevent clot formation
Atrial Fibrillation
Risk Factors
Relative Risk
History of hypertension
1.6
Heart failure and/or
reduced left ventricular
function
1.4
Advanced age
1.4
Diabetes
1.7
Coronary artery disease
1.5
Atrial Flutter
• Aetiology
– 30% have no underlying cardiovascular disease
– 30% CAD
– 30% hypertension
• Pathophysilogy
– Single reentrant circuit around the tricuspid valve
– Distinctive sawtooth ECG
Supraventricular Tachycardias
• Any tachycardic rhythm originating above the
ventricles
• It usually involves ectopic pacemaker cells or
an accessory (reentrant) pathway
• http://www.youtube.com/watch?v=Y7QdOBY
eAS4
Mechanism of Reentry
• A: slow conduction, short RP
• B: normal conduction and RP
SA Node Reentrant Tachycardia
AV Node Reentrant Tachycardia
• Aetiology
– Formation of “beta” pathway within
or alongside the node and exacerbated by
• Anxiety
• Exertion
• Caffeine, alcohol, drugs
• Signs & Symptoms
– Palpitation
– Dizziness, syncope
– Chest pain, angina (if coexisting CAD)
AV Node Reentrant Tachycardia
First Degree Block
• If the PR interval is more than 1 large square (0.2s) then this is a 1st
degree AV block
• Not associated with morbidity or mortality but foreshadows a more
severe block if MI occurs
• Risk factor = age
Second Degree Block
• A conduction delay within the AV node causing increasingly
lengthened PR intervals until the node cannot transmit the
signal to the ventricles (the Wenkebach phenominum)
• Aetiology
– Structural heart disease
– Drugs: digoxin, Na, beta and Ca channel blockers, tricyclic
antidepressants & lithium at toxic levels
– Metabolic: hyperkalaemia, hypermagnesaemia,
hyperthyroidism, Addison’s
– Enhanced vagal tone due to pain, athletes at rest
– A shit load more at
http://emedicine.medscape.com/article/161919-overview
– Mostly intranodal but poor prognosis if infranodal
Second Degree Block
Type I Wenckebach: P waves shown by arrows, lengthening PR interval
Type II: P waves shown by arrows, unpredictable non-conduction and loss of QRS
Third Degree Heart Block
• Complete interruption of conduction from the
atria
• Ventricles show escape rhythms
• Aetiology
– Infectious: Endocarditis, rheumatic fever
– Neuromuscular: muscular dystrophy
– Drugs (see 2nd degree HB)
– Rheumatic, infiltrative, metabolic, electrolyte ...
Third Degree Heart Block
BBB
• Normal P waves
• Normal PR interval
• Widening of QRS to more than 0.12s because
of delayed depolarisation of the ventricle
Ventricular Ectopic BEats
• Premature beats originating within the
myocardium
• Distinctive tall, wide beats precede the P wave
VT
• Reentrant arrhythmia as a result of scarring of
the myocardium
• The rhythm can stabilise, revert spontaneously
to sinus rhythm or lead to VF and death
Ventricular Preexitation
• Associated with WPW syndrome
• Accessory pathway Bundle of Kent allows
early ventricular depolarisation forming a
blunted Q wave called a delta wave and an
abnormal T wave (last 2 beats below)
Myocardial Ischemia
• Myocardial ischemia caused by narrowing of
the coronary arteries results in ST depression
• Below the depression is shown in the shaded
areas
ECG Online Test
• http://www.andrews.edu/~schriste/HealthTea
ching/Practice/Sinus_and_Atrial/si01.html