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IPE revision CARDIOLOGY > arrhythmias > Flashcards

arrhythmias Flashcards

1
Q

What are the causes of arrhythmias

A

Cardiac: ACS/ischaemia, HF, mitral valve disease, myocarditis, pericarditis, accessory pathways (e.g. WPW)
Non-cardiac: Electrolytes, drugs, thyrotoxicosis, anaemia

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2
Q

what are the 3 mechanisms behind the formation of arrhythmias

A

Ectopic re-entry loops

delayed depolarisation

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3
Q

state the different categories of arrhythmias

A

Brady - sinus, sick sinus, heart block

Tachy _ broad (from ventricles or SVT), narrow (down bundle of his)

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4
Q

define bradycardias

A

Heart rate <50bpm

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5
Q

what are the different types/ causes of bradycardias - briefly explain each one

A

Sinus Brady - naturally slow, Bblockers, hypothyroid, Raised ICP, MI (SAN damage)

Sick sinus - slow followed by bouts of tachy - widespread disease of the atria not just SAN

heart block: - caused by fibrosis e.g. ischaemia, haemochromatosis
1st degree - AVN delayed but still conducts each P
2nd degree type 1 - progressive delay in AVN (P-R interval) until one QRS complex is missed following P wave
2nd degree type 2 - AVN not delayed but misses conduction every 2nd or 3rd beat
3rd degree - no relationship between P wave and QRS complexes, AVN does not work at all

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6
Q

define narrow complex tachycardia

A

HR>100 with a QRS complex <120ms (3 small squares)

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7
Q

explain the different causes of narrow complex tachycardias

A
  • sinus tachy - stress, fever, pregnancy, thyrotoxicosis
  • AF
  • Flutter
  • multi-focal atrial ectopics - numerous ectopic within atria, associated with COPD
  • AVNRT (re-entry through from ventricles to atria via AVN)
  • AVRT (re-entry through from ventricles to atria via other way than AVN e.g. WPW orthodromic)
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8
Q

define broad complex tachycardias

A

HR>100, QRS>120ms

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9
Q

explain the different types of broad complex tachycardias

A
  • VT - Depolarisation coming from within the ventricles themselves at an increased rate
  • SVT - depolarisation comes from above the ventricles but not down natural pathway (e.g. bundle of his)
    types:
  • aberrancy - with increased rate one of the BB turns itself off (not present at rest)
  • pre-existing BBB - broad as only one BB conducting
  • accessory pathways - new pathway between atria and ventricles e.g. WPW antidromic
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10
Q

how do people with arrhythmias present?

A 
Palpitations
chest pain
exercise intolerance
syncope
asymptomatic
anxiety
signs of HF
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11
Q

what investigations would you suggest for someone presenting with palpitations or syncope?

A

Bloods - FBC (anaemia), U&E (K+, Mg, Ca), TFT (Hyper)
ECG / ambulatory
ECHO - heart stretch and mitral valve
Exercise stress test

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12
Q

how is sick sinus syndrome treated?

A

treat when <40bpm or symptomatic
Give IV atropine to block M2 receptors to speed heart or IV isophrenaline which stimulates B1 so speed heart
Pacemaker inserted (to treat brady)
B blockers to slow heart (blocks remaining ectopics)

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13
Q

when is sick sinus syndrome NOT treated?

A

when HR >40bpm and asymptomatic

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14
Q

what are the causes of heart block?

A

ischaemia, fibrosis (SLE, RA), haemochromotosis, pharma e.g. b blockers, CABG (also aortic valve replacement - damaged in tavi)

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15
Q

when does heart block require pacing?

A

When 2nd degree type 2 or 3rd degree
3rd degree requires pacing as ventricular rates are slow and unreliable (type 2 likely to develop into type 3 and why it needs replacing)

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16
Q

what drugs can aid in heart block?

A

Atropine (for transient heart block)

adrenaline

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17
Q

describe ECG changes seen in wolf Parkinson white

A

Delta waves present (slow rise R)

P-R interval shortened as depolarisation begins through the accessory pathway whilst AVN hold conduction

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18
Q

explain why WPW can be both broad and narrow complex tachycardia

A

Both are re-entry loop (does not always happen in WPW, only when cause of tachy)

Broad as can have accessory route which does not follow the usual pathway (bundle of his) then back up AVN

Narrow as down the normal pathway AVN then back up to atria through the accessory route

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19
Q

describe steps in managing a narrow complex tachycardia

A

A-E, IV access and give o2, call help

if unstable straight to DC cardioversion

if stable: try Valsalva manoeuvre, carotid massage
if unsuccessful try pharma: give adenosine 6mg up to 25mg to block AVN (rhythm)
treat underlying rhythm with fleccanide or B blockers

in long term ablate accessory pathway - or treat with flecanide long term

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20
Q

how does adenosine help narrow complex tachycardia?

A

blocks AVN

dosage of 6mg up to 25mg

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21
Q

what are side effects of adenosine ?

A

bronchospasm
impending doom
chest pain
flushing

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22
Q

how does flecanide help narrow complex tachycardia

A

voltage gated Na channel blocker

slows down action potential - prevents excitability of myocytes (can also slow AVN)

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23
Q

how is a broad complex tachycardia treated?

A

A-E, peripheral IV access, O2, call for help

unstable patient - straight to DC cardiovert
then begin amiodarone

stable patient:
give controlled o2 therapy, correct electrolytes, give IV amiodarone, continue ECG monitoring

for all long term:
continue amiodarone for 7 days
long term bisoprolol
consider implanting automatic cardiac defibrillator

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24
Q

what ECG changes are found in VT?

A

Concordance - every ECG lead has same deflection in QRS (either up or down)

Capture beats and fusion beats - narrower than usual ventricular QRS

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25
What is AF?
atria chaotically fibrillate instead of contracting - unsynchronised myocyte contraction originates in left atria usually
26
explain ECG changes associated with AF
absent P waves with wobbly baseline QRS is irregularly irregular tachycardia sometimes
27
what are the causes of AF?
Mnemonic = MITRAL mitral valve disease IHD/HTN thyroid disease rheumatic fever alcohol excess / metabolic disturbance (K+) lung disease (P.E, pneumonia), LV hypertrophy
28
what are the complications of AF?
Ventricular tachy (SVT) - AVN increases responsiveness so high rate of depolarisation reaches ventricles reduced CO - partly due to SVT, and atria do not contract so less filling Thromboembolism - stasis (esp atrial appendices) leads to thrombi formation which can lead to: - stroke - mesenteric infarct - limb ischaemia
29
describe the symptoms of AF
Direct - asymptomatic, chest pain/palpitations, irregularly irregular pulse indirect - (related to cause) - valve disease = breathless, murmur - HF = hepatomegaly, raised JVP, decreased BP - thyroid = goitre - infection = fever
30
what investigations would you carry out in someone with AF?
bloods - FBC, U&E, TFTs, troponin, BNP ECG ECHO - valve disease, stretch
31
what is atrial flutter?
ectopic atrial beats cause re-entry circuit in the atria atrial myocytes conduct in synchrony but at an increased rate without rest atrial rate at approx. 300bpm
32
describe ECG changes seen in atrial flutter
lots of P waves very close to one another = saw tooth | get a pattern of P to QRS that can be 2:1, 3:1 or 4:1 etc
33
what are the causes of atrial flutter?
ischaemia HTN cardiomyopathy heart valve abnormalities
34
what are signs/symptoms of atrial flutter?
``` palpitations - flutter feeling in the chest SoB syncope raised JVP anxiety tachycardia ```
35
what are the complications of atrial flutter?
relatively benign condition strain on heart from tachy clot formation risk
36
how is acute unstable AF managed?
ABCDE Do tests and keep ECG monitoring on throughout start treating the cause Emergency DC cardioversion (do not worry about starting anticoagulation before, although heparin should be started)
37
how is acute stable AF managed that occurred less than 48 hours ago managed?
Can wait a few hours to see if spontaneously resolves (70% of cases) rate control - verapamil/bisoprolol Rhythm control - electrical or pharma: - no IHD then amiodarone or flecanide - amiodarone if evidence of structural/IHD when starting rhythm control also start heparin due to risk of coagulation
38
how is acute stable AF that occurred more than 48 hours ago managed?
- Rate control only - delay rhythm control until anticoagulation has occurred for 4 weeks prior to cardioverting - INR >2 - Can check atrial appendices for thrombi via trans-oesophageal USS - continue anticoag at least 4 weeks post-cardioversion and then monitor for need of long term anticoagulation using CHADsVaSc
39
describe management of chronic AF
Rate control - b blocker/Ca channel locker usually 1st line Digoxin considered if congestive HF Rhythm control - Sotalol first line amiodarone/flecanide (preferred in paroxysmal, young and symptomatic AF - can do pill in pocket approach) Anticoagulation - warfarin/NOAC offered Catheter ablation and pacing - ablate AVN and insert ventricular pacemaker
40
what is cardioversion and compare the different types?
intention to put heart back into sinus rhythm - electrical = DC cardioversion can be attempted up to 12 months of AF onset - Pharma = amiodarone, flecanide less successful but no need for sedation
41
what are the contraindications to cardioversions
AF >1year AF likely to reoccur e.g. cause still there or structural Cardioversion already failed no of times Anticoag is contraindicated
42
define paroxysmal, persistent and permanent AF
Paroxysmal = most common, terminates 1-7days persistent = >7days Permanent = >1 year
43
what is the CHADSVAS score
``` risk of thromboembolitic event C = CCF (1) H = HTN (1) A2 = >65 (1), >75 (2) D = Diabetes (1) S2 = Stroke/TIA/Thrombus (2) Va = Vascular disease (1) Sc = Sex female (1) ```
44
what is HASBLED?
``` risk likelihood of bleeding: H = HTN A = abnormal liver/renal function S = Stroke B = Bleeding L = labile INR E = Elderly D = drugs/alcohol score of >3 = high risk of bleeding ```
45
what other way can the risk of stroke in AF be reduced other than anticoagulation?
surgically remove the atrial appendices as 90% clots form there
46
where do AF and flutter originate?
AF = left atria from smooth muscle of pulmonary veins flutter = right atrium
47
how can you tell if there is left axis deviation or right axis deviation on ECG?
left axis deviation = aVL > I right axis deviation = III > aVF
48
what are the causes of left and right axis deviation?
hypertrophy or conduction defects such as WPW, hemi-blocks
49
what is p mitrale?
Bifid P waves | caused by left atrial hypertrophy as a result of HTN, or mitral valve disease
50
what is p pulmonale?
Peaked P waves anything causing right atrial hypertrophy COPD, CHD, tricuspid stenosis, pulmonary HTN
51
what is the normal PR interval?
120-200ms
52
what are the causes of tall and wide QRS complex?
tall = ventricular hypertrophy wide = BBB, ventricular ectopics, WPW
53
what causes ST elevation?
MI, pericarditis (concave + widespread over all leads)
54
what causes ST depression and how can ST depression be defined?
Ischaemia defined as: - >1mm in 2 consecutive limb leads - >2mm in 2 consecutive chest leads
55
when is a T wave inverted?
NSTEMI
56
when is a T wave tall?
Hyperkalaemia or MI
57
when do we see U waves?
Hypokalaemia
58
How do you treat WPW?
Flecanide to control arrhythmias | or ablate the accessory pathway
59
What is the Valsalva manoeuvre?
strain and hold breath in supine position | on release of strain the vagal activity should reduce
60
how do you treat atrial multi-focals (ectopics)
often due to COPD - hypoxia and hypercapnia | correct this and ectopics will correct
61
What is the difference between Defibrillation and Cardioversion
Defibrillation = non-synchronised random administration of shock (given any time in cardiac cycle - emergency) Cardioversion = synchronised administration of shock (given at certain point in cycle e.g. after QRS to shock heart back into normal rhythm)
62
What are the indications for defibrillation?
Emergencies: - Pulseless VT - VF
63
what are the indications for electrical cardioversion?
- SVT - AF - VT with a pulse
64
Do defibrillation and electrical cardioversion require sedation?
Defibrillation = with or without, done in emergency setting Cardioversion = almost always sedated first

IPE revision CARDIOLOGY (9 decks)

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