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Medicine > Cardiovascular: arrythmias > Flashcards

Cardiovascular: arrythmias Flashcards

arrythmias

1
Q

what is the definition of a narrow complex tachycardia?

A

ECG >100bpm
QRS complex duration <120ms
which occur when ventricles are depolarised via the normal conduction pathways

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2
Q

what are the differentails for a narrow complex tachycardia?

A

regular narrow complex tachycardia

irregular narrow complex tachycardia which include:
1- normal variant- sinus arrythmia (rate changes with insp/exp), sinus rhythm with frequent ectopic beats

2- AF
3- Atrial flutter with variable block. Atrial rythmn regular, vent rhythm irreg

4- multifocal atrial tachycardia- p wave morphology and p-p intervals vary, associated with copd

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3
Q

how do you manage narrow complex tachycardia?

A

1- identify + treat underlying rhythm

2- if AVNRT or AVRT suspected transiently block AVN

3- some cases cause symptomatic episodes of sufficient severity + frequency to warrant more invasive treatment like ablation therapy for accessory pathways

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4
Q

how can you transiently block AVN in suspected AVNRT or AVRT?

A

1- vagal manoeuvres- carotid sinus massage, valsalva manoeuvre eg blowing into a syringe

2- IV adenosine

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5
Q

when the underlying rhthm is sinus tachycardia secondary to dehydration, how do you treat?

A

IV fluids

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6
Q

when the underlying rhthm is multifocal sinus tachycardia secondary to COPD, how do you treat?

A

correct hypoxia and hypercapnia

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7
Q

when the underlying rhthm is focal atrial tachyardia secondary to digoxin toxicity, how do you treat?

A

digoxin-specific antibody fragments

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8
Q

when the underlying rhthm is AVRT secondary to WPW, how do you treat?

A

flecainide or
propafenone or
amiodarone

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9
Q

what is holiday heart syndrome and which rythm disorders commonly present?

A

binge drinking in someone without any clinical evidence of heart disease can result in acute cardiac rythm and/or conduction disturbances

recreational marijuana has similar effects

SVT supraventricular tachyarrhthmia
AF (consider when new AF with no structural heart defect)

prognosis good- advise against excessive alcohol use

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10
Q

what is the normal conduction pathway?

A

SA node -> AV node -> Bundle of His -_ depolarises ventriuclar myocardium from bottom/apex to top/outflow tract

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11
Q

what is the pathway in sinus tachycardia?

A

conduction occurs as normal
impulses initiated at higher frequency

causes:

  • infection, pain, dehydration, bleed, systemic vasildation in sepsis
  • drugs- caffeine, nicotine, salbutamol
  • anaemia, fever, PE, co retention, autonomic neuropath y
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12
Q

what is the pathway in focal atrial tachycardia

A

group of atrial cells act as a pacemaker, out-pacing the SA node

p wave morphology is different to sinus

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13
Q

what is the pathway in atrial flutter?

A

electrical activity circles the atria 300x/min

gives sawtooth baseline

AV node passes some of these impulses on resulting in ventricular rates that are factors of 300- 150, 100, 75

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14
Q

what is the pathway in atrioventriuclar re-entry tachycardia AVRT?

A

an accessory pathway eg in WPW allows electrical activity from ventricles to pass to resting atrial myocytes, creating a circuit

atria- AVN- ventricles- accessory pathway- atria

orthodromic direction results in narrow QRS complexes as ventricular depolarisation is triggered via bundle of His- orthodromic conduction

antidromic direction results in broad QRS complexes

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15
Q

what is the pathway in AVNRT/atrioventricular nodal re-entry tachycardia?

A

circuits form within AVN
this causes narrow complex tachycardias
very common

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16
Q

what is the pathway in junctional tachycardia?

A

cells in AVN become pacemaker, giving narrow QRS complexes as imulses reach ventricles through normal routes

p waves may be inverted and late

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17
Q

what is the pathway in bundle branch block

A

any of the other conditions can result in broad copmlex tachyardias if there is a bundle branch block

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18
Q

what is the pathway in ventricular tachycardias VT?

A

this can result from circuits, similar to atrial flutter

or result from focuses of rapidly-firing cells

broad QRS
when circuit is in action and its plane rotates, ECG shows broad complex tachycardia with regularly increasing and decreasing amplitudes-_ torsades de pointes

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19
Q

in supraventricular arrythmias, the initial depolarisation originates from…?

A

atria or around AV node

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20
Q

in ventricular arythmies, the inital depolarisation originates from…?

A

ventricles

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21
Q

where is the accessory pathway in AVRT?

A

between the atria and ventricles

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22
Q

where is the accessory pathway in AVNRT?

A

between the atria and AV node

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23
Q

what is in the ECG to diagnose supraventricular tachycardias (AVRT/AVNRT)?

A

regular, narrow QRS complex tachycardia
rate 150-200
p waves abnormal

in WPW p wave is upside down and follows closely after QRS

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24
Q

what are the clinical features of supra ventricular tachyarrythmias?

A

recurrent attacks of rapid regular palpitations that last a few mins to hours/days (new onset post-MI suggests VT)

mild faintness- decreased JVP +/- low BP, varying intensity 1st Heart sound

unconscious- cardiogenic shock, very low BP

syncope if VT transient

sudden cardiac death

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25
Q

what is the treatment for supraventricular tachyarrythmias?

A

aim is to slow conduction through AV node

1- vagotonic manoeuvres that increase vagal tone- valsalva manoeuvre, carotid sinus massage

2- drug IV adenosine, beta blockers

3- radiofrequency ablation

26
Q

what is the accessory pathway involved in WPW?

A

an accessory pathway conducts atrial depolarisations directly into ventricular myocardium
this bypasses AV node

pre-exciation and AV reciprocating tachycardias and pre-excited AF may occur

27
Q

untreated AF heart rate is usually…?

A

100-150bpm

28
Q

what are the different classifications of AF?

A

paroxysmal
persistent (medical cures)
permanent (medical treatment doesn’t keep them in sinus rhythm)

29
Q

AF ECG diagnosis involves…?

A

QRS rate fast and irregularly irregular

no p waves are visible

baseline may be flat or show fast, small depolarisations

30
Q

what are the clinical features of AF?

A

fast irregular palpitations- sudden onset, defined duration, sudden offset (if no underlying heart disease just this)

breathlessness (impaired LV fx/HF)
exercise capacity may be limited
embolic events- stroke (late), limb ischaemia, mesenteric ischaemia
syncope- rare- underlying sinus node disease

31
Q

what are the cardiac causes of AF?

A

any structural heart disease- especially mitral stenosis

pericarditis

32
Q

what are the metabolic causes of AF?

A

alcohol

thyrotoxicosis

33
Q

what are the pulmonary causes of AF?

A

pneumonia
PE
COPD

34
Q

what are the predisposing causes of VT (monomorphic)?

A

old/new MI
LV hypertrophy
HF
cardiomyopathy

35
Q

what are the causes of VT (polymorphic)?

A

genetic disease eg hereditary long QT syndrome- jervell-lange-nielsen syndrome, romano-ward syndrome (ion channel mutations)

drugs that prolong QT interval (tricyclic antidepressants, amiodarone, quinidine, stall, antihsitamines )

acute myocardial ischaemia

hypo- kalaemia, magnesaemia, calcaemia

bradycardia- any cause

36
Q

what is an idiopathic cuase of AF?

A

increasing age

more common in men than women

37
Q

what is the treatment for AF (+ atrial flutter)?

A

1- rate control
digoxin (slows rate at rest), Bb (slows rate at exercise), calcium channel antagonists

2- rhythm control
amiodarone, flecainide, sotalol
DC cardioversion if AF present for <1yr + heart normal
otherwise ablation

3- anticoagulation
CHA2DS2-VASC. Score 2 or more use warfarin INR target 2.5-3 or antithrombotic like dabigatran/rivaroxaban
use HASBLED score to see risk of bleeding. 3 or more use with great caution.

after cardio version CHADSCVASc score is high, stay on anticoagulant fro 2-3yrs becaues risk of recurrent AF is high

38
Q

what is the ECG diagnosis for atrial flutter?

A

QRS rate is exactly 150 if alternate flutter waves conducted (atrial flutter with 2-1 block) or divisbles of flutter rate eg 100 (3 to 1), 75 (4 to 1)

sawtooth flutter waves instead of p waves most obviously in leads II III aVF and VI

*if regular tachycardia has constant rate of exactly 150 always think at. flutter even if flutter waves not obvious (can be obscured by QRS/T waves)

39
Q

what are the clinical features of atrial flutter?

A

pulse rate usually 150 + regular

asymptomatic or
rapid palpitation
breathlessness
or be in HF

40
Q

what is the pathogenesis of atrial flutter

A

atrial flutter is the result of a macro re-entry circuit moving anti-clockwise around R atrium

atria depolaries in rapid coordinated fashion

41
Q

what is seen on ECG for ventricular tachycardias?

A

QRS complexes broad wtih an abnormal shape

VT always suspected when patient known to have heart disease (esp recent/remote MI) and regular tachy with broad QRS complex

42
Q

what is the difference between monomorphic VT and polymorphic VT?

A

monomorphic VT- uniform QRS morphology, rate 120-190, maybe dissociated p waves as evidenc eof independent atrial activity

polymorphic- less regular, more choatic, characteristic phasic variation in QRS morphology- torsades de pointes
polymorphic VT is unstable and degenerates early on into VF

43
Q

what are the clinical features of VT?

A

pulse rate fast, may be weak - no pulse palpable

can be in acute HF, severely compromised, cardiac arrest (pulseless VT)

or be well with rapid palpitation or breathlessness - still have a risk of haemodynamic deterioration

44
Q

how do you treat pulseless VT or impending cardiovascular collapse?

A

DC cardio version - either immediately or after urgen anaesthesia/sedation

45
Q

how do you treat haemodynamically stable VT?

A

IV lidocaine (lignocaine)

or amiodarone
never use multiple drug combos
if drugs unsuccessful use DC cardioversion

46
Q

how do you treat polymorphic VT?

A

DC cardioversion
IV magnesium
correction of underlying metabolic/electrophysiological abnormality

slow heart reates prolong the QT interval and may worsen polymoprhic VT. so increasing HR by pacing often prevents or reduces incidenc eof polymorphic VT

47
Q

how do you prevent future episodes of VT?

A

long term drug therapy- BB, amiodarone, ACEi, spironolactone to improve LV fx +maintain K+

revascularisation- CABG or PCI for severe coronary disease

ICDs- implantable cardiovertor defibrillators- indicated for survivors of cardiac arrest and in symptomatic VT with impaired LV fx

48
Q

if patients survive VF, it is important to find underlying cause. Full cardiac and coronary imaging takes place. what are some causes?

A

IHD- acute MI, critical coronary stenosis treated with complete revascularisation, no new ischaemia but old MI scar treat with ICD

structural heart disease- cardiomyopathies- need ICD usually

channelopathies eg hereditary long QT syndrome, Brugada’s syndrome

rare- WPW syndrome with complicating AF + very hihg HR; acquired long QT syndromes eg starvation

49
Q

what are the ECG features for 1st degree AV block

A

prolonged PR interval

50
Q

what is the site/cause of impaired conduction in 1st degree AV block

A

AV node

may be fucntional due to drugs or high vagal tone

51
Q

what is the natural history/treatment for 1st degree AV block

A

if functional- progression unsuual
if due to AV node disedase- progression common

observation only

52
Q

what are the ECG features of 2nd degree AV block Mobitz 1/wenckeback

A

some p waves not conducted

progressive PR interval prolongation leads to dropped beat

53
Q

what is the site/cause of impaired conduction for 2nd degree AV block Mobitz 1/wenckeback

A

AV node

may be functional due to drugs or high vagal tone

54
Q

what is the natural history/treatment for 2nd degree AV block Mobitz 1/wenckeback

A

may be benign

but often needs pacemaker

55
Q

what are the ECG features of 2nd AV block mobitz II?

A

only every 2nd or 3rd p wave is conducted

56
Q

what is the site/cause of impaired conduction for 2nd degree mobitz II?

A

structural AV node/bundle of his disease

57
Q

what is the natural history/treatment for 2nd degree heart blcok mobitz II?

A

always progresses to CHB 3rd degree

early permanent pacemaker

58
Q

what are the ECG features for 2rd degree CHB?

A

no p waves conducted

p waves and ventricular escape rhythm completely indpendent- AV dissocation

59
Q

what is teh site/cause of impaired conduction for 3rd degree CHB?

A

strucutral disease of AV node +/- conducting system

60
Q

what is the natural history/treatment of 3rd degree CHB?

A

unreated death <6 weeks
urgent pacemaker
immediate pacemaker if history of syncope or HR <35

Medicine (3 decks)

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