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Cardiovascular > fibrillations > Flashcards

fibrillations Flashcards

1
Q

define superventricular tachycardia

A

supreventricular tachyarrthymias with uncoordinated atrial electrical activation and consequently ineffective atrial conduction

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2
Q

what is paroxysmal AF?

A

recurrent AF that reverts spontaneously

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3
Q

what is persistent AF?

A

if recurrent AF reverts spontaneously and needs pharmacological/ cardioversion to manage

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4
Q

what are the RF for AF?

A

age. hypertension, diabetes, obstructive sleep aponea, CAD, valve disease, alcohol, congenital heart disease, lung disease

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5
Q

what is the most common type of cardiac arrhthymia?

A

atrial fibrillation

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6
Q

how does cardiac remodelling contribute to the pathophysiology of AF?

A

particularly in the atria
results in structural/ electrical chnages that causes a derrnaged rhythm.
changes in myocytes/ ECM, fibrous tissue deposition

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7
Q

how does the unsynchronised firing pathophysiology result in AF?

A

initiating triggers from an ectopic focus in the atria - usually pulmonary veins .

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8
Q

what are the consequences of the unsynchronised firing?

A

turbulent and abnormal blood flow through heart decreasing effectiveness in pumping blood, increasing likelihood of thrombus formation in atria, most commonly left atrial appendage

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9
Q

what manual diagnostic test can you perform to detect AF?

A

manual pulse palpitations to assess for irregular pulse

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10
Q

describe the clinical presentation of AF

A

dyspnoea, palpitations, syncope/ dizziness, chest discomfort, stroke/ TIA, anxiety, fatigue, symptomatic hypotension <90mmHg

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11
Q

what do you look for on an ECG showing AF?

A

irregular RR intervals
absence of distinct repeating P waves
irregular atrial activations

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12
Q

if you suspect paroxysmal AF, would monitoring would you use?

A

24hr electrical activity monitor

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13
Q

what is the general management of chronic AF?

A

personalised package of care
stroke awareness
rate control meds
contacts with helplines
psychological advice
up to date education
anticoagulants
networking charities for support

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14
Q

what medications is for stroke prevention in regards to AF management?

A

direct- acting oral anticoagulant

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15
Q

name some anticoagulants used to treat AF

A

apixaban, dabigatran, edoxaban, rivaroxaban

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16
Q

if a patient is contraindicated to anticoagulants but need medication for stroke prevention following AF, what do you use?

A

vitamin K antagonist

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17
Q

if a patient is already using anticoagulants and experienced a MI, what drugs are best to use as well?

A

anti-platelets

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18
Q

what are 1st line drugs in managing AF (rate and rhythm)

A

beta blocker
non-dihydropyridine calcium channel blocker - dilitizam/ verpamil

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19
Q

if a patient with chronic AF does little amounts of physical exercise - what drug is best?

A

digoxin monotherapy

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20
Q

what are second line drug management for AF?

A

combination of b blocker, diltiazem, dogoxin

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21
Q

what do antiarrthymic drug therapy aim to do?

A

long term rhythm control

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22
Q

what drugs are antiarrhythmics?

A

flecainde
propafenone
dronedarone
amiodarone
pill pocket strategy

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23
Q

what antiarrhythhymics do you not give if known ischaemia/ structural heart disease?

A

class 1c - flecainide/ propafedone

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24
Q

amiodarone is used in patients with AF that always have…?

A

left ventricular impairment
heart failure

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25
Q

what is the pill pocket strategy?

A

only taking antiarrhythymic drugs when needed eg after doing something that triggers it eg exercise/ caffeine intake

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26
Q

when would cardioversion be suitable?

A

AF symptoms presenting >12hrs

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27
Q

when would you start amiodarone before cardioversion?

A

ideally 4 weeks prior - chronic AF

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28
Q

what is cardioversion?

A

a device that delivers low-energy shocks to the heart

29
Q

when would you do left atrial ablation?

A

if the drugs were unsuccessful

30
Q

describe left ablation process

A

uses small burns/ freezes and cause scarring on the inside of the heart to help break up electrical signals

31
Q

after undergoing cardioversion, how long should be on antiarrhythymics for?

A

3 months following

32
Q

what is atrial fibrillation better care?

A

ABC
Anticoagulants/ avoid stroke
Better symptom management
Cardiovascular and comorbidity optimisation - lifestyle changes

33
Q

in acute AF and someone is haemodynamically instable, what is best course?

A

emergency electrical cardioversion

34
Q

what medications are best to control rate/ rhythm in acute AF?

A

flecainade/ amiodarone

35
Q

what drugs are contraindicated for acute AF?

A

Mg2+/ CCB

36
Q

what drug types should be given to acutely AF patients?

A

antiarrthymics and anticoagulants - heparin

37
Q

what is atrial fibrillation?

A

heart rhythm problem where atria beats irregularly

38
Q

what is supraventricular fibrillation?

A

has electrical signals orginating at or above the AN - defines by narrow QRS <120ms adn a heart rate >100bpm

39
Q

what is the pathophysiology of supraventricular fibrillation?

A

orthodromic re-entry phenomenom
tachycardia is secondary to normal anterograde electrical conduction from atria to AVN
signal can also go from ventricles back to atria
narrow QRS - ventricles being activated prior to AVN

40
Q

how does the ventricles get depolarised before the AVN in supraventricular fibrillation?

A

may develop an ectopic foci of electrical activity within the atria, AVN, ventricles
impulse conduction - conduction blocks and forms re-entrant circuits
impulse formation - enahnced autorhtyhmaticity (pacemaker away from SAN) or triggered activity activity during repolarisation

41
Q

what are re-entrant circuits within SVT?

A

continuous wave of depolarisation in circular path - depolarising wave returns to original site

42
Q

name 5 examples of SVT rhythyms

A

sinus tachycardia, atrial tachycardia, atrial flutter, atrial fibrillation, atrioventricular nodal re-entrant tachycardia, atrioventricular re-entrant tachycardia

43
Q

describe the symptoms of SVT?

A

anxiety, palpitations, chest discomfort, light-headed, syncope, dyspnea
shock, hypotnesion, signs of HF
can be asymptomatic but tachycardia seen within screening

44
Q

what are the diagnostic signs on a ECG of SVT?

A

narrow QRS complex, regular tachycardia
HR - 180-220 bpm
no P waves

45
Q

what investigation is crucial in SVT?

A

find initial cause
assess for haemodynamic stability

46
Q

what symptoms would suggest haemodynamic instabilities?

A

hypotension, hypoxia, SoB, chest pain, evidence of poor end organ failure perfusion, altered mental status

47
Q

what is the management for a haemodynamic unstable patient with SVT?

A

immediate synchronised cardioversion
adensosine

48
Q

what is the initial management for a haemodynamically stable patient with SVT?

A

Vagal manoeuvres can be attempted
carotid sinus massage
adenosine

49
Q

what are valsalva movements?

A

popping ears motion by holding nose

50
Q

how do you perform a carotid sinus massage?

A

patients neck must be extended and turned away - firm pressure applies for linger than 5 seconds

51
Q

what is the second line management of SVT?

A

CCB/ B blockers
CCB must by di-hydropidines

52
Q

if pharmacological actions do not work to treat SVT, what are next options?

A

catheter ablation
pacemaker

53
Q

what is ventricular tachycardia?

A

wide complex tachycardia
>100bpm

54
Q

what is non sustained VT?

A

lasts less than 30s and presents tachycardia with tachyarrthymias with >3 beats of ventricular origin

55
Q

what is sustained VT?

A

> 30s, haemodynamically unstablility occurs in less than 30s from tachycardia

56
Q

what is monomorphic VT?

A

stable QRS morphology

57
Q

what is polymorphic VT?

A

has changing or multiform QRS - torsades de pointes

58
Q

what is bidirectional VT?

A

beat to beat alteration in QRS frontal plane
linked to digitalis toxicity/ catecholaminergic polymorphic VT

59
Q

what is the aetiology of VT?

A

usually ischaemic HD
can be structural HD, channelopathies, infiltrative cardiomyopathy, electrolyte imbalance
illicit drugs
hypokalemia followed by hypomagnesemia

60
Q

what is the pathophysiology of VT?

A

enhanced normal automaticity/ abnormal automaticity

61
Q

what causes the pathology of SVT?

A

activity triggered by early/ late afterdepolarisation and re-entry
in acute MI - transient ischaemia causes hyperkalaemia and triggers partial depolarisation
injury currents between infarcted tissue and healthy myocardium and triggers spontaneous activity

62
Q

when history taking how would you differentiate between VF and SVT?

A

those VF are more likely to be older

63
Q

what would an ECG show if a patient had SVT?

A

broad complexes
fast HR

64
Q

other than ECG, what other tests can be used to diagnosis VT?

A

stress test
bloods - potassium, magnesium, calcium

65
Q

how would you manage non sustained VT and asymptomatic?

A

no therapies

66
Q

how would you manage non sustained VT but was symptomatic?

A

b blockers
CCBs 2nd line

67
Q

how do you manage sustained monomorphic VT that is haemodynamically unstable

A

advanced cardiac life support

68
Q

what do haemodynamically stable VT patients need?

A

antiarrthymic medication

69
Q

when would a VT patient get an implanted cardiac defibrillator

A
  • ischaemic HD and survive a cardiac arrest
    if they have haemodynamically unstable/ sustained VT

Cardiovascular (14 decks)

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