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Cardio Block > 3- cardiac arrhythmias > Flashcards

3- cardiac arrhythmias Flashcards

1
Q

where are the anatomical conduction system parts of the heart?

A
  • SA node in upper RA
  • AV node
  • His bundles in between atria & ventricles
  • bundle branches down between ventricles
  • purkinje fibres spreading out around muscles
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2
Q

what are names of arrhythmias generally based on?

A
  • anatomical side or chamber of origin e.g. atrial or ventricular
  • Mechanism or pathway eg ‘fibrillation’, or ‘ re-entry tachycardia’
  • tachycardia - anything more than 100 bpm and bradycardia is anything less than 6o bpm
  • Can occurs as single beats (ectopy) or continuously (persistent/sustained) or repeated episodes of limited duration (paroxysmal or non-sustained)
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3
Q

what is supraventricular?

A

non-specific term used to describe arrhythmias whose origin is above ventricle

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4
Q

where do supraventricular arrhythmias originate from?

A

originate from above the ventricle, i.e., sinoatrial node, atria, AV node or His bundle

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5
Q

what is appearance of supraventricular arrhythmias on ECG?

A
  • atrial depolarization is visible by rapid P-waves (for atrial fibrillation)
  • ventricular depolarisation is visible by narrow QRS complex - indicating that the electrical impulses are conducted through normal conduction pathway (unless there’s a block in His-purkinje fibres)
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6
Q

where does ventricular tachycardia arrhythmia originate from?

A

ventricular myocardium (common) or fascicles (bundle branches) of the conducting system (uncommon)

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7
Q

what does ventricular tachycardia look like on ECG?

A

a wide QRS as the arrhythmia path is outside the fast conducting His-Purkinje system, and therefore conducts slower, resulting in a longer depolarization time

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8
Q

what is ventricular tachycardia?

A

an arrhythmia characterized by a rapid and regular or irregular heartbeat originating from the ventricles (myocardium or bundle branches) of the heart

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9
Q

what are common types of atrial tachycardia?

A
  • atrial fibrillation (irregular heart rhythm characterized by chaotic and rapid electrical activity in the atri)
  • atrial flutter (regular heart rhythm characterized by a rapid and organized electrical activity in the atria)
  • ectopic atrial tachycardia (arrhythmia characterized by abnormally fast heartbeats originating in the atria)
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10
Q

what are common types of bradycardia?

A
  • sinus bradycardia (abnormally slow heart rate originating from the sinus node)
  • sinus pauses
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11
Q

what are sinus pauses?

A
  • Sinus pauses, also known as sinus arrest, occur when there is a temporary interruption in the normal activity of the sinus node.
  • During a sinus pause, there is a brief period where the sinus node fails to generate an electrical impulse, resulting in a pause in the heart’s rhythm
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12
Q

what is atrial flutter?

A
  • Atrial flutter is characterized by a regular and organized atrial rhythm.
  • The atria contract at a rapid and regular rate
  • the ventricular response can be regular or irregular, depending on the conduction through the atrioventricular (AV) node.
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13
Q

why does atrial flutter occur?

A

often occurs due to re-entry circuits within the atria, where electrical signals circulate in a loop

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14
Q

what does ectopic mean?

A

an abnormal heart rhythm that originates from a location other than the heart’s normal pacemaker, the sinoatrial (SA) node

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15
Q

what are types of ventricular arrhythmias?

A
  • ectopic or premature ventricular complexes (a beat occurs before expected timing of next normal heartbeat - originate from outside normal conduction pathway)
  • ventricular tachycardia (fast, regular & sustained)
  • ventricular fibrillation (fast, chaotic, irregular beats - ventricles quiver)
  • asystole (absence of electrical activity in the heart, form of cardiac arrest)
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16
Q

what happens in ectopic ventricular arrhythmia?

A

ectopic ventricular arrhythmia = abnormal site of electrical activity in ventricles is firing at faster rate than SA node

  • ectopic ventricular focus = region in ventricles that generates electrical impulse
  • when ectopic ventricular focus firing at faster rate than SA node, it overtakes & surpassess the normal heart rate set by SA node →electrical impulses generated by ectopic focus is dominant source controlling heart rhythm
  • when SA node initiates normal electrical impulse and it encounters other electrical impulses, there’s a conflict
  • the faster firing ectopic focus can suppress the normal pacemaker activity of SA node →heart rhythm dominated by impulses originating from ectopic ventricular focus →arrhythmia where ventricles contract at different rate
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17
Q

what does ventricular tachycardia look like on ECG?

A
  • in VT, QRS complex may have different appearance due to abnormal origin of electrical impulse
  • SA node could still be firing →this means that intermittently there could be normal electrical impulses and sometimes they can escape down purkinje fibres and generate impulse that bypasses the abnormal ventricular rhythm
  • when SA node escapes down purkinje fibres, the QRS complex on ECG is normal

*this is sign of ventricular tachycardia = intermittent normal QRS

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18
Q

what is atrioventricular node arrhythmia?

A

AV node arrhythmia can be complete or partial block of electrical impulses between atria & ventricles
(AV node = specialized group of cells in heart that is the only connection between atria & ventricles)

*AV arrhythmia allows some beats and not others = intermittent

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19
Q

what does ECG look like for AV arrythmia?

A
  • In the arrhythmia we see prolongation of conduction - this means that normal passage of electrical signals from atria →ventricles takes longer
  • PR interval may initially appear normal but if prolongation excessive then first degree AV block
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20
Q

what is PR interval on ECG?

A

represents time taken for electrical impulse to travel from atria through AV node into ventricles

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21
Q

what are the different degrees of AVN block?

A
  • First degree AVN block = slow conduction (long PR interval)
  • Second degree = intermittent, PR interval may be varying
  • Complete or third degree= complete non-conduction
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22
Q

what happens when people have accessory pathway?

A

leads to 2 types of re-entrant tachycardias:
1. micro-circuit = involves short circuit within AV node
2. macr-circuit = abnormal circuit involving both accessory pathway & AV node, it’s located far away from AV node

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23
Q

what are causes of arrythmias?

A
  1. abnormal anatomy that allow re-entrant circuits (accessory pathways, congenital heart defects)
  2. autonomic nervous system (sympathetic stimulation like stress, exercise, hyperthyroidism and increased vagal tone increasing bradycardia)
  3. metabolic
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24
Q

what are metabolic causes of arrhythmia?

A
  • hypoxia: chronic pulmonary disease, pulmonary embolus
  • ischaemic myocardium; acute MI, angina
  • electrolyte imbalances: K+, Ca2+, Mg2+
  • inflammation: viral myocarditis
  • drugs: direct electrophysiologic effects or via ANS
  • genetic: mutations of genes encoding cardiac ion channels e.g. congenital long QT syndrome
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25
Q

what can lead to ectopic beats occurring?

A
  • ectopic beats can occur due to altered automaticity (change in normal rhythm of the heart) e.g. ischaemia, increase in catecholamines
  • ectopic beats can also occur from triggered activity, e.g. digoxin, long QT syndrome
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26
Q

what does re-entry mean?

A

re-entrant circuit = an abnormal electrical pathway within the heart that allows an electrical impulse to circulate continuously, leading to an arrhythmia

  • re-entry requires more than 1 conduction pathway, each with different speed of conduction (depolarisation) and recovery of excitability (refractoriness)
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27
Q

what are examples of re-entry arrythmias?

A
  • atrioventricular nodal re-entry tachycardia (AVNRT)
  • atrioventricular re-entry tachycardia (AVRT) which is associated with an accessory pathway tachycardia e.g.Wolf Parkinson White syndrome
  • myocardial scar from previous myocardial infarction
  • congenital heart disease.
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28
Q

what are the 2 main categories for mechanisms responsible for cardiac arrythmias?

A

(1) enhanced or abnormal impulse formation (ie, focal activity)

(2) conduction disturbances (ie, reentry)

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29
Q

what happens when enhanced automaticity occurs in the SA node?

A

it can lead sinus tachycardia = an increase in heart rate

- This can be physiological, due to increased sympathetic tone during exercise, or pathophysiological, due to hypovolemia, ischemia, or electrolyte disturbances.
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30
Q

what is enhanced automaticity of pacemaker cells?

A

increased ability of pacemaker cells to generate spontaneous electrical impulses

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31
Q

what are the 3 main mechanisms that cause enhanced automaticity?

A
  1. an increased rate of phase 4 (resting phase) depolarization
  2. a negative shift in the threshold potential (meaning less stimulus required to reach threshold)
  3. a positive shift in the maximum diastolic potential (means membrane potential starts at a higher level making it easier to reach threshold and initiate APs)
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32
Q

what can increase phase 4 slope and what does that do?

A

phase 4 = resting membrane potential
- increasing phase 4 slope = Increasing the rate of spontaneous depolarization which increases the heart rate

increase slope by:
- Hyperthermia (elevated temp)
- Hypoxia (deficiency in O2 in tissues)
- Hypercapnia (increased CO2 level in blood)
- Myocardial stretch (stretching or enlargement of heart muscle)
- Sympathetic nervous system

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33
Q

what can decrease phase 4 slope and what does that do?

A

phase 4 = resting membrane potential.
decreasing phase 4 slope = decreasing rate of depolarisation which slows heart rate

decreases phase 4 slope:
- Hypothermia (decreased temp)
- Hyperkalaemia (elevated potassium levels in blood)
- parasympathetic nervous system

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34
Q

what are afterdepolarizations?

A

afterdepolarizations are premature depolarisations that occur in the terminal phase of the AP

2 types:
1. during phase 2 or 3 = early after depolarisation, EAD
2. after AP in phase 4 = delayed afterdepolarization, DAD

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35
Q

what is circus re-entry?

A

Re-entry can occur in the presence of an obstacle (tissue that disrupts normal propagation like scar, structural abnormality etc), obstacle creates pathway around itself allowing AP to travel in circular loop (circus re-entry) and result in a resulting in a self-perpetuating circuit

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36
Q

when does re-entry occur? (in terms of electrical signals)

A

Re-entry occurs when an action potential fails to extinguish itself (continues to circulate in heart tissue) and reactivates a region that has recovered from refractoriness (period when heart cell can’t respond to another stimulus) and this leads to a self sustaining where a circuit is established that allows the electrical signal to continuously circulate, creating a loop which can lead to arrhythmias

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37
Q

what are requirements for re-entry?

A
  • More than one conduction pathway, these pathways must be connected and provide a circuit through which an impulse can circle.
  • The pathways have different speed of conduction (depolarization) and recovery of excitability (refractoriness), such that an area can be blocked (unidirectional block).
  • Central blocking by a core of tissue that is completely blocked and allows the impulse to loop around in the surrounding excitable tissue.
  • Block can be caused by structural abnormalities: accessory pathways, scar from myocardial infarction, congenital heart disease, or functional i.e. conditions that depress conduction velocity or shorten refractory period promote functional block, e.g. ischaemia, drugs
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38
Q

what does arrhythmia propagation (how abnormal heartbeat spreads through heart) require?

*what is needed for abnormal heartbeat to spread through heart?

A

triggers & substrates

  • Triggers e.g., EADs (early after depolarisation) and DADs (delayed after depolarisation) which can produce ectopic beats
  • Substrate = electrophysiological abnormalities predisposing to re-entry, including increased heterogeneity of conduction or repolarization

*Triggers can produce abnormal heartbeats, and substrates set the stage for these abnormal beats to spread in the heart

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39
Q

what are symptoms of arrhythmia?

A
  • Palpitations, ”pounding heart”, “skipped beat”, ‘flip-flopping’
  • Dyspnoea
  • Faintness: “presyncope”
  • Transient loss of consciousness; ”Syncope”
  • Angina
  • Heart failure if persistent and fast
  • Anxiety
  • NB sometimes arrhythmia are asymptomatic (usually AF or ectopy)
40
Q

is tachycardia life-threatening?

A

can be - depends on how it affects cardiac output & blood pressure e.g. if haemodynamically stable or unstable

unstable = syncope & cardiac arrest and sudden death

stable = hypotension and reduced coronary circulation to angina and heart failure

41
Q

what investigations would you want to do for tachycardia?

A
  • 12 lead ECG (during SR and in tachycardia ideally)
  • Bloods: full blood count, Biochemistry, thyroid function
  • Chest X-ray (to assess heart size, heart failure)
  • Echocardiogram to look for structural heart disease
  • Stress ECG = Look for myocardial ischaemia, exercise related arrhythmias
  • 24-hour ECG Holter monitoring to assess for
    • correlation of heart rhythm to symptoms
    • Asymptomatic arrhythmia
  • Event recorder: (patient activated during symptoms of arrhythmia)
  • Electrophysiological (EP) study
    • Induce clinical arrhythmia to study mechanism and map arrhythmia
42
Q

what are pre-excitation waves on ECG?

A

they are called delta waves and are caused by ventricular depolarisation through the accessory pathway

43
Q

what are the types of ECG?

A
  • exercise ECG
  • 24hr holter ECG - to assess for paroxysmal arrhythmia & To link symptoms to underlying heart rhythm
  • echocardiogram - like ultrasound to look at heart structure, valve disease, LV, RV dilation, hypertrophic cardiomyopathy, previous MI scar if aneurysm
  • electrophysiological study
    • To trigger the clinical arrhythmia and study its mechanism/pathways
    • Opportunity to treat the arrhythmia by delivering radiofrequency ablation to extra pathway
44
Q

what is respiratory sinus arrythmia?

A

the natural variation in heart beat as we go through respiratory cycle

  • variation in heart rate, due to reflex changes in vagal tone during respiratory cycle
    • inspiration reduces vagal tone & increases heart rate
45
Q

what is heart rate for sinus bradycardia?

A
  • <60 bpm
  • can be normal (physiological), especially in athletes
46
Q

what can cause sinus bradycardia?

A
  • drugs like beta-blockers
  • dysfunction of sinus node disease
  • conditions affecting channels in heart (channelopathies) like long QT syndrome can contribute
47
Q

what is treatment of sinus bradycardia?

A
  • atropine
  • pacing (pacemaker) if haemodynamic compromise, which is when it causing too many issues like hypotension, CHF, angina, collapse
48
Q

what is heart rate for tachycardia?

A
  • HR > 100 beats/min
  • can be normal (Physiological) like in Anxiety, fever, hypotension, anaemia
49
Q

what is treatment of sinus tachycardia?

A

Treat underlying cause like with B-adrenergic blockers

50
Q

what can regular supraventricular tachycardia be caused by?

A
  • AV nodal re-entrant tachycardia (AVNRT)
  • AV re-entrant tachycardia (via an accessory pathway) (AVRT)
  • Ectopic atrial tachycardia (EAT) - abnormal firing outwith SA
51
Q

what is management for acute supraventricular tachycardia?

A
  • Increase vagal tone: valsalva, carotid massage
  • Slow conduction in the AVN
  • IV Adenosine
  • IV Verapamil
52
Q

what is chronic management for supraventricular tachycardia?

A
  • Avoid stimulants
  • Electrophysiologic study and Radiofrequency ablation (first line in young, symptomatic patients)
  • Beta blockers
  • Antiarrhythmic drugs
53
Q

what is radiofrequency catheter ablation (RFCA)?

A

Selective localised cautery of cardiac tissue to prevent tachycardia, targeting either an automatic focus or part of a re-entry circuit

54
Q

what happens in radiofrequency catheter ablation?

A
  • ECG Catheters placed in heart via femoral veins.
  • Intra-cardiac ECG (Electrocardiograms, EGMs) recorded during sinus rhythm, tachycardia and during pacing manoeuvres to find the location and mechanism of the tachycardia
  • Catheter placed over focus / pathway and tip heated to 55-65C to cause localised cautery
55
Q

what are causes AV node conduction disease? (heart block)

A
  • Ageing process
  • Acute myocardial infarction
  • Myocarditis
  • Infiltrative disease (Amyloid, sarcoid)
  • Drugs (B-adrenergic blockers & Calcium channel blockers)
  • Calcific aortic valve disease
  • Post-aortic valve surgery
  • Genetic : Lenegre’s disease, myotonic dystrophy
56
Q

what are the degrees of AVN block?

A

1st degree = not really block - there is still conduction to ventricles it just takes longer, PR interval longer than normal

2nd degree = intermittent block, 2 types:
1. progressive lengthening of PR interval until dropped beat, usually vagal origin
2. pathological, may progress to complete heart block (3rd degree), usually 2:1 or 3:1, permanent pacemaker indicated

3rd degree = complete block, no AP get through AV node

57
Q

what are types of pacemakers?

A
  • Single chamber (paces the right atria or right ventricle only)
  • Dual chamber (paces the RA and RV)
    • Maintains A-V synchrony (preserves atrial kick)
    • Used for AVN disease
58
Q

when is ectopy more likely to symptomatic?

A

when associated with reduced BP

59
Q

what are causes of ventricular ectopics?

A
  • structural causes - LVH, heart failure, myocarditis
  • metabolic - ischaemic heart disease, electrolytes
  • inherited cardiac conditions - hypertrophic cardiomyopathy
60
Q

what is management of ventricular ectopics?

A

= investigate cause & treat accordingly

  • beta blockers, ablation of ectopic focus, anti-arrhythmic drugs
61
Q

what are ECG characteristics that help define ventricular tachycardias?

A
  • The QRS complexes are rapid, wide, and distorted.
  • The T waves are large with deflections opposite the QRS complexes.
  • The ventricular rhythm is usually regular.
  • P waves are usually not visible.
  • The PR interval is not measurable.
  • A-V dissociation may be present.
  • V-A conduction may or may not be present.
62
Q

what is acute ventricular tachycardia treatment?

A
  • Direct current cardioversion (DCCV) if unstable.
  • If stable: consider initial pharmacologic cardioversion with anti-arrhythmic drugs, in meantime prepare for DCCV.
  • Correct triggers; Look for causes
    • Electrolytes
    • Ischaemia
    • Hypoxia
    • Pro-arrhythmic medications (eg drugs that prolong the QT interval eg., sotalol).
63
Q

what is long term treatment for ventricular tachycardia?

A
  • Correct ischaemia if possible (coronary artery disease management , including PCI, bypass surgery)
  • Optimise chronic heart failure therapies.
  • Anti-arrhythmic drugs to date have been shown to be ineffective and are associated with worse outcomes.
  • Implantable cardiovertor defibrillators (ICD) if life threatening and high risk of recurrence.
  • VT catheter ablation
64
Q

what are implantable cardiovertor defibrillators (ICD)?

A

they are devices implanted that detect & treat bradyarrhythmias as well as ventricular tachycardia and ventricular fibrillations
- they can discriminate supraventricular tachycardias and other atrial tachyarrhythmias to reduce the incidence of inappropriate ventricular therapies, including inappropriate shocks

they treat by:
ventricular tachycardia termination by,
- antitachycardia pacing (ATP)
- low-energy cardioversion
- defibrillation for ventricular tachyarrhythmias (VT/VF).
- Treatment in the atrium AND the ventricle also includes pacing for bradycardia

65
Q

what does a wide QRS tachycardia with history of coronary artery disease or heart failure mean?

A

ventricular tachycardia until proven otherwise

66
Q

what problem is mostly associated with structural heart disease? (chronic heart failure or coronary artery disease)

A

most ventricular arrhythmias

67
Q

what is purpose of prescribing anti-arrhythmic drugs?

A

are ineffective on survival, but are often used together with ICDs (Implantable Cardioverter-Defibrillator) to reduce symptoms

68
Q

what is general practice management of acute arrhythmia management?

A
  • Treat acute arrhythmia to
    • stabilise the patient
    • alleviate symptoms
  • Correct triggers; look for causes
    • Electrolyte imbalance K+, Mg2+
    • Ischaemia
    • Hypoxia
    • Pro-arrhythmic medications (eg drugs that prolong the QT interval eg., sotalol)
    • consider genetic channelopathy if in a young person
  • Optimise treatment of underlying disease e.g. heart failure, hypertension.
  • Interventions: Ablation, CIEDs (Cardiac Implantable Electronic Device), anti-arrhythmic drugs
69
Q

what are key characteristics of atrial fibrillation?

A
  • chaotic & disorganised atrial activity →irregular heartbeat
  • can be paroxysmal, persistent or permanent (chronic)
  • most common sustained arrhythmia
  • can be symptomatic or asymptomatic
  • incidence increases with age
70
Q

what are associated diseases with atrial fibrillation? (think genetic, lifestyle, metabolic, inflammation etc)

A
  • congenital heart disease
  • genetic: familial, AF, channelopathies
  • Infection : septicaemia, chest infections
  • Inflammation: myocarditis, pericarditis, cardiac surgery, myocardial infarction, obesity
  • Vascular : coronary artery disease, hypertension
  • Metabolic: thyroid disease, electrolyte disturbance
  • Structural: valve disease especially mitral valve, heart failure, left ventricular hypertrophy, atrial tumors (myxoma)
  • Lifestyle: alcohol excess, obesity, high endurance athletes
71
Q

what is lone (idiopathic) atrial fibrillation?

A

atrial fibrillation when there’s an absence of any heart disease & no evidence of ventricular dysfunction
(diagnosis of exclusion)

*remember could be genetic if in young person e.g. prugada syndrome, congenital long QT syndrome

72
Q

what are symptoms of atrial fibrillation?

A
  • palpitations
  • pre-syncope
  • syncope
  • chest pain
  • dyspnea
  • sweatiness
  • fatigue
73
Q

what are different patterns of atrial fibrillation?

A

paroxysmal = begins suddenly & stops, lasting less than 48 hours, Often recurrent

persistent = An episode of AF lasting greater than 48 hours, which can still be cardioverted to normal sinus rhythm but unlikely to spontaneously revert to normal sinus rhythm

permanent = Inability of pharmacologic or non-pharmacologic methods to restore normal sinus rhythm

74
Q

what is mechanism of atrial fibrillation?

A

ectopic foci in muscle sleeves in the ostia of pulmonary veins - interrupts normal rhythm and suppresses it

75
Q

what is speed of beats in atria & ventricles like in atrial fibrillation?

A

ventricles can be beating fast or slow (depends on condition)

atrial fibrillation can also be slow (not always fast) - the trai quiver instead of contract

76
Q

what does atrial fibrillation ECG look like?

A

P & T waves not visible - instead wavy deflections replace the entire isoelectric line between QRS complexes which occur irregularly because of inherent delay in AV node

77
Q

what is pathophysiology of atrial fibrillation?

A
  • lost atrial kick and decreased filling times (reduced diastole) →reduced cardiac output
  • can result in congestive heart failure, especially in the presence of stiff ventricle e.g. LVH
    • pulmonary edema not unusual when stiff ventricle
78
Q

what is management of atrial fibrillation?

A

2 options:
1. rhythm control
- objective to keep them in sinus rhythm
2. rate control (for when restoration of sinus rhythm not possible)
- accept they’re in atrial fibrillation but maintain and control

*Anti-coagulation essential in both treatment strategies if high risk for thromboembolism

79
Q

what pharmacological therapy can slow down AVN conduction?

A
  • digoxin
  • beta blockers
  • verapamil, diltiazem

*if pharmacologic rate control not successful or tolerated, ablation of the AVN and implantation of a permanent pacemaker ‘ablate and pace is a last resort

80
Q

what can be done to restore normal sinus rhythm after AF?

A
  • Pharmacologic cardioversion (anti-arrhythmic drugs e.g. amiodarone)
  • Direct Current Cardioversion (DCCV)
81
Q

what can be done to maintain normal sinus rhythm after AF?

A
  • Anti-arrhythmic drugs
  • Catheter ablation of atrial focus/ pulmonary veins
  • Surgery (Maze procedure)
82
Q

what are ways to terminate atrial fibrillation?

A
  • sometimes tops on it’s own (spontaneous)
  • can use drug (pharmacological cardioversion with anti-arrhythmic drugs, not very effective)
  • electrical cardioversion (90% effective) by direct current (DCCV)
83
Q

what do anti-arrhythmic drugs do?

A

act through electrophysiological mechanisms by blocking the ionic currents across cell membranes that create the action potentials

84
Q

what is class 1 anti-arrhythmic drugs?

A

Class 1: reducing Na channel current (AP phase 0)
→Lignocaine, quinidine, flecainide, propafenone

85
Q

what is class 2 anti-arrhythmic drugs?

A

Class II: B-Adrenergic antagonists (AP phase 4)
→Propranolol

86
Q

what is class 3 anti-arrhythmic drugs?

A

Class III: action potential prolongation & K+ channel
(AP phase 3)
→Amiodarone, sotalol
→DRONEDARONE

87
Q

what is class 4 anti-arrhythmic drugs?

A

Class IV - Ca channel antagonists
(AP phase 2)
→Verapamil

88
Q

what is purpose of radiofrequency ablation in AF?

A

To maintain sinus rhythm - by ablating AF focus (usually in pulmonary veins)

For rate control - ablation to the AVN to stop fast conduction to the ventricles

89
Q

what is left atrial catheter ablation?

A
  • Isolate triggers in the pulmonary veins by pulmonary in LA vein isolation
  • Safe and more effective at preventing AF than pharmacologic therapy
90
Q

when is risk of thrombo-embolic stroke increased in AF?

A
  • Thyrotoxicosis
  • Hypertrophic cardiomyopathy
  • Mitral valve disease: especially mitral stenosis
  • Non valvular AF with 2 or more of the following
    • Female
    • Age >75
    • Hypertension
    • Heart failure
    • Previous stroke/ thromboembolism
    • CAD
    • Diabetes
91
Q

what is done as stroke prevention in AF?

A
  • oral anti-coagulation is effective at prevention of stroke in AF
  • long term anticoagulation is recommended in high risk groups:
    • OAC: warfarin, apixabam, rivaroxaban, dabigatran
    • NB: warfarin is the only oral anti-coagulant in mitral valve disease(lack of clinical trial efficiency evidence for the newer oral anticoagulants)
92
Q

what is used to assess stroke risk in AF?

A

CHADS2 - VASc score

congestive heart failure
hypertension
age >75 (2pts)
diabetes
S2 - prior TIA or stroke (2pts)
Vascular disease
Age 65-74
Sex Category

0 male or 1 female = low risk (not anti-coagulant)
1 male = moderate (oral anticoagulant considered)
2 or greater (oral anticoagulant

93
Q

what are characteristics of atrial flutter?

A
  • rapid & regular form of atrial tachycardia
  • paroxysmal or persistent pattern
  • sustained by a macro-reentrant circuit
  • circuit is usually confined to RA
  • episodes can last from seconds to years
  • chronic atrial flutter usually progresses to AF
  • carries risk of thrombo-embolic stroke
94
Q

what does counterclockwise flutter mean in atrial flutter?

A
  • With counterclockwise flutter, a macro-reentrant circuit exists. This circuit is sustained by a critical isthmus.
  • Induction of counterclockwise flutter can be accomplished with rapid atrial pacing and/or the introduction of multiple premature beats near the low septum.
95
Q

how can you terminate counterclockwise atrial flutter?

A

with rapid atrial pacing, cardioversion, or with the use of medications, such as Ia, Ic, or class 3 antiarrythmic drugs.

96
Q

what are treatment options for atrial flutter?

A

RF ablation (80-90% long term success)

might try pharmacological therapy (doesn’t work as well as ablation):

  • Slow the ventricular rate
  • Restore sinus rhythm
  • Maintain sinus rhythm once converted

Cardioversion

OAC for prevention of thromboembolism

97
Q

What is intermittent normal QRS a sign of?

A

Ventricular tachycardia

Cardio Block (34 decks)

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