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year 3 exam 1 > arrythmias and treatments > Flashcards

arrythmias and treatments Flashcards

1
Q

what is a arrythmia

A

abnormality in heart rate or rhythm

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2
Q

arrythmia epidemiology

A

5.3% UK

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3
Q

types of arrythmia based on location in the heart

A

supraventricular - above/at or in AV
ventricular

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4
Q

arrythmia symptoms

A

dizzy
palpitations
chest pain
fatigue
lose consciousness
cardiac arrest

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5
Q

how are arrythmias diagnosed

A

ECG

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6
Q

how are arrythmias managed pharmacologically

A

treat underlying cause
Vaughn williams drugs

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7
Q

what is radiofrequency ablation/cryoablation

A

Radiofrequency energy or freezing destroys tissue at point of arrythmia

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7
Q

how are arrythmias managed non-pharmacologically

A

electrical cardioversion
radiofrequency ablation
pacemaker
defibrillators
ICD - internal cardioversion defibrillators

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7
Q

what is electrical cardioversion

A

DC delivered via controlled electric shock across chest wall- anticoag 3 weeks prior and 4 weeks post

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8
Q

what is a pacemaker

A

Deliver small electrical impulses to myocardial tissue if detects inappropriate rhythm

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9
Q

what is defibrillation

A

Delivery of electric shock to myocardium via chest wall (VT/VF)

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10
Q

what is ICD - internal cardioversion defibrillator

A

Implanted into high risk patients with resistant VT’s to monitor rate & rhythm, Initially deliver rapid rate impulses (faster than arrhythmia) to try to regain control and then slow down, If fails, deliver internal electric shock

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11
Q

what is bradycardia

A

HR <60BPM

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12
Q

what are the different types of bradycardia

A

sinus bradycardia - SA node fires slowly
sinus node disease - SA node fails to generate electrical impulse
AV node disease/heart block - failure of AV node to conduct electrical impulses to ventricles

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13
Q

what are the three types of heart block

A

1st degree - long PR interval
2nd degree - not all Ps have QRS
3rd degree - QRS very slow

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14
Q

how is acute bradycardia managed

A

atropine to increase HR

15
Q

how is chronic bradycardia managed

A

discover underlying cause
permanent pacemaker

16
Q

what is tachycardia

A

HR >100BPM

17
Q

what types of supraventricular tachycardia can happen

A

sinus tachycardia - fast, normal rhythm *can be infection, anaemia, low BP related)
sinus node re-entry tachycardia
AF
atrial flutter - AF but less frequent - saw tooth pattern
AV junction tachycardia
Wolff-Parkinson White syndrome - bypasses AV node (600bpm)

18
Q

what are the types of ventricular tachycardia

A

ventricular tachycardia - >5 ventricular beats consecutively
ventricular ectopics
torsade’s des pointes - QT prolongation
ventricular fibrillation - rapid uncontrolled contraction - deadly

19
Q

what are some causes of torsade’s des pointes

A

congenital
hypokalaemia
hypomagnesaemia
lithium

20
Q

how is rhythm controlled in tachycardia

A

amiodarone
200mg tds 7/7, 200mg bd 7/7, 200mg od maintenance

21
Q

how is rate controlled in tachycardia

A

digoxin
500mcg x 2 six hours apart, 125mcg maintenance

22
Q

side effects of amiodarone

A

bradycardia
taste disturbances
grey skin
liver/thyroid dysfunction

23
Q

digoxin side effects

A

N&V, blurred vision, anorexia, bradycardia

24
Q

what are the Vaughn Williams antiarrhythmic drugs

A
  1. sodium channel blockers - flecainide
  2. beta blockers - atenolol
  3. potassium channel blockers - amiodarone
  4. CCBs - verapamil
25
Q

how do class 1 Vaughn Williams antiarrhythmic drugs work

A

sodium channel blockers, slow depolarisation before contraction - slows HR

26
Q

how do class 2 Vaughn Williams antiarrhythmic drugs

A

beta blockers, extends phase 4, less SA node firing

27
Q

how do class 3 Vaughn Williams antiarrhythmic drugs work

A

potassium channel blockers, slows repolarisation, longer action potential and longer contraction

28
Q

how do class 4 Vaughn Williams antiarrhythmic drugs work

A

CCBs, lengthens plateau phase, reduces force and rate of contraction

29
Q

what two non-Vaughn Williams antiarrhythmic drugs are used for arrythmias

A

adenosine
digoxin

30
Q

adenosine MOA

A
  • Binds to adenosine receptor 1 (GPCR Gi receptor)
    • Gi inactivated adenylyl cyclase
    • Decrease in cAMP
    • Decrease in action potential firing from SA node
31
Q

digoxin MOA

A
  • Inhibits Na/K ATPase and reverses Na/Ca exchanger
    • Increased Na in cardiomyocyte - reverses Na/Ca exchanger so increased Ca in cell
    • Increased Ca = increased contraction force

year 3 exam 1 (44 decks)

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