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Cardiology > Arrythmias > Flashcards

Arrythmias Flashcards

1
Q

A patient is pulseless and unresponsive in A+E. What are the 4 possible rhythms that they are likely to have and which rhythms mean they can be shocked?

A

Shockable:
Ventricular tachycardia
Ventricular fibrillation

Non-shockable:
Pulseless electrical activity
Asystole

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2
Q

What determines whether patient with tachycardia is stable or unstable? Why is this important to establish?

A

Unstable tachycardia= reduced CO

  • shock (<90mmHg + >100 HR)
  • chest pain or signs of ischaemia on ECG
  • HF
  • syncope

Unstable patients need to be cardioverted ASAP

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3
Q

Tachycardias can be narrow complex or broad complex. How are they distinguished on an ECG? Which tachycardias below in each category?

A

Narrow= <3 small squares

  • AF
  • Atrial flutter
  • Supraventricular tachycardia

Broad= >3 small squares

  • Ventricular tachycardia
  • Ventricular flutter

I.e. problems with atria= narrow and problems with ventricles= broad

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4
Q

What is the pathophysiology behind atrial flutter?

A

Re-entrant rhythm occurs where electrical signal re-circulates in the atria rather than into ventricles after the AVN due to extra electrical pathways

Signal becomes self-perpetuating, which leads to atria contracting at 300bpm

Signal goes to ventricles once every 2 laps of atrial circuit leading to 150 bpm in ventricles

Consequences on ECG:

  • sawtooth pattern produce= lack of isoelectric baseline between p-waves
  • not every P wave is associated with QRS complex
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5
Q

What conditions increase the risk of atrial flutter developing?

A

Hypertension
IHD
Cardiomyopathy
Thyrotoxicosis

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6
Q

What is the treatment for atrial flutter?

A

(Similar to atrial fibrillation)
Rate and rhythm control= beta blockers

Treat underlying condition i.e. hypertension

Radiofrequency ablation of re-entrant rhythm

Anticoagulation= DOACs

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7
Q

What are the 3 possible causes of irregularly irregular pulse?

A

Atrial fibrillation

Variable block atrial flutter

Benign ectopic beat

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8
Q

What causes supraventricular tachycardia and how can it be identified on an ECG?

A

Electrical signals re-enter the atria from ventricles leading to signal passing down AVN and back into ventricles to stimulate another ventricular contraction

Narrow complex= <3 small squares i.e. QRS closely followed by T wave which is closely follow by QRS

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9
Q

How is stable SVT managed? What needs to be done whilst SVT is being managed?

A

Vagal manoeuvres:
-Valsalva manoeuvre= blowing on syringe i.e. blowing against resistance (increases intrathoracic pressure and increases the vagal tone to slow conduction through the AV node and prolongs AV nodal refractory period

-Carotid sinus message

Adenosine

CCB i.e. verapamil (used as adenosine alternative)

Direct current cardioversion if treatment fails

NOTE: need to ensure that patient is hooked up to continuous ECG to monitor effects of management

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10
Q

What is the MOA of adenosine and why is it used to manage SVT?
What is the treatment dosage and when is it contraindicated?
What do you need to warn the patient of before giving?

A

Blocks AVN to slow cardiac conduction and interupt AVN/accessory pathways to enable heart to reset sinus rhythm in SVT i.e. can induce asystole or bradycardia

6mg bolus, then 12 mg, then 12mg
-needs to be given bolus to ensure it reaches the heart with enough impact to interrupt the pathways

Avoid in patients with: asthma/COPD/HF/heart block/severe hypotension

Need to warn about possible feeling of impending doom or like they are dying due to adenosine inducing asystole/bradycardia

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11
Q

What is the difference between SVT and VT?

A

Dependent on location of the origin of tachycardia

SVT= atria

VT= ventricles

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12
Q

Why does VT occur and what are the signs someone might be experiencing VT?

A

Can occur due to damage or scar tissue formation which creates abnormal pathways in ventricles
I.e. MI/cardiomyopathy/HF/myocarditis/heart valve disease

Presentation:

  • lower BP
  • syncope
  • chest pain
  • SOB
  • cardiac arrest (when progressed to ventricular fibrillation)
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13
Q

How would you manage stable VT?

A

300 mg amiodarone IV bolus over 1 hr

900 mg amiodaron IV over 24 hrs

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14
Q

What is the management of pulseless VT or unstable VT?

A

Cardioversion

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15
Q

What is the MOA of amiodarone?

Why must it be given via central line rather than cannula?

A

Blocks potassium currents that cause repolarisation of heart muscle
I.e. acts as anti-arrhythmic to restore heart rhythm to normal

Can cause phlebitis if given through cannula due to being irritant so central line required as it is much larger reduces the risk of phlebitis

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16
Q

How is Torsades de Pointes different from regular VT?

How is it managed?

A

Polymorphic VT with height of QRS complexes getting progressively smaller and then progressively bigger again

TDP= recurrent contractions of ventricles without normal repolarisation

Need to treat to prevent progression to VT:

  • correct cause i.e. medications or electrolyte disturbance
  • magnesium infusion
  • cardioversion if VT occurs
17
Q

What are the SE of amiodarone? What tests need to be done before patient started on this drug?

A

Can comprise liver function
Can cause lung fibrosis
Can alter thyroid function
Can increase sunlight sensitivity i.e. increased risk of burns
Corneal deposits (resolve when stop taking drug)

Need to establish baseline liver, lung and thyroid function

18
Q

What are ventricular ectopics and how might patients with these present?

A

Random electrical discharge leads to premature ventricular beat

Patient experiences random, brief palpitation

19
Q

When should particular concern/attention be payed to patient presenting with ectopic beats?

A

History of MI= increased risk of developing dangerous arrythmia

In case of bigeminy= ectopic occurring after every sinus beat

20
Q

How are ectopic beats managed?

A

Bloods check:

  • FBC= signs of anaemia
  • U+E= electrolyte disturbance
  • TFT= assess thyroid function
21
Q

What is Wolff-Parkinson White syndrome? What ECG changes would you expect to see?

A

Extra-electrical pathways develop which connect the atria and ventricles which enables alternative route for electrical signals to travel other than AVN

Short PR interval
Wide QRS complex
Delta wave= slurred upstroke

22
Q

What are the main types of heart block? What is the difference between them?

A

1st degree:

  • delayed AVN conduction= prolonged PR interval
  • each P wave followed by QRS complex (no dropping of QRS complexes)

2nd degree:

  • some signals DON’T make it from AVN to ventricles= prolong PR AND not all P waves followed by QRS
  • mobitz type 1= progressively prolonged PR then QRS dropped
  • mobitz type 2= constant PR with set ratio of P:QRS i.e. 3:1 block due to intermittent failure of AVN

3rd degree= complete HB
-no relationship between P and QRS

23
Q

When is treatment required for heart block and what does this involve?

A

Patient unstable or risk of asystole (mobitz type 2 or 3rd degree)

Atropine 500 mcg IV (antimuscarinic to inhibit PNS meaning no longer limiting HR)

Additional:

  • another dose atropine
  • inotropes (NAd)
  • defibrillator
24
Q

When is antiarrhythmic medications contraindicated in patient with WPW and why?

A

When they have also developed AF +/- atrial flutter

Promote conduction of electrical signals through the accessory pathway due to antiarrhythmics blocking/reducing the conduction of signals via AVN
I.e patients can develop polymorphic wide complex tachycardia

25
Q

When are patients indicated to have a pacemaker fitted? What is its function?

A

Patients at high risk of asystole= mobitz type 2 or complete HB

Electrode fed into RA or RV to provide direct electrical stimulation to correct rhythm

26
Q

What are the classifications of anti-arrhythmic drugs?

A

Class 1= sodium channel blockers= decreases velocity of AP which can suppress tachycardias
Eg= Quinidine/Lidocaine/Flecainide

Class 2= beta-blockers= blocks binding of Ad/NAd to decrease chronotropy (HR), ionotropy (contractility)
Eg=Bisoprolol/Atenolol/Metoprolol (all cardioselective)

Class 3= potassium channel blockers = delays repolarisation and increase QT interval i.e. effective at stopping re-entry mechanisms
Eg= Amiodarone

Class 4= calcium channel blockers = decreased force of myocardium contraction and prolong repolarisation at AVN i.e. helps to block re-entry mechanisms
Eg= verapamil

27
Q

What is the difference between dihydropyridines and non-dihydropyridines?

A

Dihydro (“pine”) = high SM/vascular selective i.e. primarily use as antihypertensives

Non-dihydro (verapamil)= selective for myocardium i.e. used for angina and arrhythmias

NOTE: diltiazem is non-dihydro which sits in-between verapamil and dihydro

28
Q

When is verapamil (cardio selective non-dihydropyridine) contraindicated and why?

A

Conduction defects or HF due to systolic dysfunction

Due to risk of verapamil causing excess bradycardia and impaired electrical conduction (AVN block) and can can worsen HF due to decreased contractility exacerbated already suppressed function of myocardium

29
Q

Why can’t veramapril and bisoprolol not be used together?

A

Increased risk of hypotension and bradycardia

I.e. increased risk of cardiac arrest if patients given both

30
Q

What are the main types of arrhythmias?

A 
SVT
VT 
Atrial flutter 
Atrial fibrillation 
Ectopic beats 
AVNRT (AVN re-enterant tachycardia)
31
Q

Where do the wires of a pacemaker go in the heart? How can you differentiate from CRT?

A

In right atria and right ventricle

CRT has insulatory sleeve on wire

Cardiology (15 decks)

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