Arrhythmias Flashcards

(47 cards)

1
Q

What key considerations should be had in the ABCDE approach to a tachycardia with pulse

A
  1. Give oxygen if SpO2 < 94%
  2. Obtain IV access
  3. Monitor ECG, BP, SpO2, record 12-lead ECG
  4. Identify and treat reversible causes e.g. electrolyte abnormalities, hypovolaemia causing sinus tachycardia
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2
Q

What life-threatening features should you be aware of when managing tachycardia?

A
  1. Shock
  2. Syncope
  3. Myocardial ischaemia
  4. Severe heart failure
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3
Q

In the presence of life threatening features, how would you manage tachycardia?

A

Synchronised DC shock up to 3 attempts (sedation or anaesthesia if conscious)

If unsuccessful:
* Amiodarone 300 mg IV over 10–20 min
* Repeat synchronised DC shock

(in 2015 resus flowchart, next step is 900mg IV amiodarone over 24hr, but this is not present in 2021 resus flowchart)

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4
Q

In the absence of life-threatening features, what ECG feature is used to group tachycardias

A

QRS duration.
* >0.12s (3 small squares) –> broad complex tachycardia
* <0.12s (“) –> narrow complex tachycardia

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5
Q

Broad complex tachycardia with irregular rhythm

A

Atrial fibrillation with bundle branch block
- treat as for irregular narrow complex

Polymorphic VT (e.g. torsades de pointes)
- give magnesium 2g over 10 min

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6
Q

Broad complex tachycardia with regular rhythm

A

If VT (or uncertain rhythm):
* Amiodarone 300 mg IV over 10–60 min

If previous certain diagnosis of SVT with bundle branch block/ aberrant conduction:
* Treat as for regular narrow complex tachycardia

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7
Q

Narrow complex tachycardia with irregular rhythm

A

Probable atrial fibrillation:
* Control rate with beta-blocker
* Consider digoxin or amiodarone if evidence of heart failure
* Anticoagulate if duration > 48 h

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8
Q

Narrow complex tachycardia with regular rhythm

A
  1. Vagal manoeuvres
  2. If ineffective:
    * Give Adenosine (if no pre-excitation)
    – 6 mg rapid IV bolus
    – If unsuccessful, give 12 mg
    – If unsuccessful, give 18 mg
    * Monitor ECG continuously
  3. If ineffective:
    * Verapamil or beta-blocker
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9
Q

If initial treatment is ineffective for regular tachycardias (both broad and narrow), what can you do next?

A

If ineffective:
* Synchronised DC shock up to 3 attempts
* Sedation or anaesthesia if conscious

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10
Q

What conditions are supraventricular tachycardias (SVTs)

A
  • Atrial flutter/tachycardia
  • Atrio-ventricular nodal re-entry tachycardia (AVNRT)
  • Atrio-ventricular re-entrant tachycardia (AVRT)
  • Atrial fibrillation (irregular, but also generated SVT)
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11
Q

Atrial flutter

A
  • Substrate originates from atrial chambers (focal or re-entrant)
  • Saw-tooth appearance
  • Counter-clockwise circuit going through the atria
  • Treatment: ablation
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12
Q

AFib: types

A

either first detected episode, paroxysmal, persistent or permanent

  1. first detected episode (irrespective of whether it is symptomatic or self-terminating)
  2. recurrent episodes, when a patient has 2 or more episodes of AF.
    - If episodes of AF terminate spontaneously then the term paroxysmal AF is used. Such episodes last less than 7 days (typically < 24 hours).
    - If the arrhythmia is not self-terminating then the term persistent AF is used. Such episodes usually last greater than 7 days
  3. in permanent AF there is continuous atrial fibrillation which cannot be cardioverted or if attempts to do so are deemed inappropriate. Treatment goals are therefore rated control and anticoagulation if appropriate
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13
Q

Afib: signs and symptoms

A

Symptoms
- palpitations
- dyspnoea
- chest pain

Signs
- an irregularly irregular pulse

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14
Q

Afib: investigations

A

ECG is essential to make the diagnosis as other conditions can give an irregular pulse, such as ventricular ectopics or sinus arrhythmia

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15
Q

Afib: key management aspects

A

There are two key parts of managing patients with AF:
1. Rate/rhythm control
2. Reducing stroke risk

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16
Q

What is the difference between rate and rhythm control

A

rate control: accept that the pulse will be irregular, but slow the rate down to avoid negative effects on cardiac function

rhythm control: try to get the patient back into, and maintain, normal sinus rhythm. This is termed cardioversion. Drugs (pharmacological cardioversion) and synchronised DC electrical shocks (electrical cardioversion) may be used for this purpose

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17
Q

Situations where rhythm control considered over rate

A

coexistent heart failure, first onset AF or where there is an obvious reversible cause.

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18
Q

Drugs used in rate control

A

First-line: beta-blocker or a rate-limiting calcium channel blocker (e.g. diltiazem)

If one drug does not control the rate adequately NICE recommend combination therapy with any 2 of the following:
a betablocker
diltiazem
digoxin

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19
Q

Risk of cardioversion - stroke
1. Important safety measure

A

The moment a patient switches from AF to sinus rhythm presents the highest risk for embolism leading to stroke. Imagine the thrombus formed in the fibrillating atrium suddenly being pushed out when sinus rhythm is restored.
1. short duration of symptoms (less than 48 hours) or be anticoagulated for a period of time prior to attempting cardioversion.

20
Q

CHA2DS2-VASc
1. Treatment suggestion based on score

A
  • determine the most appropriate anticoagulation strategy

C Congestive heart failure 1
H Hypertension (or treated hypertension) 1
A2 Age >= 75 years 2
Age 65-74 years 1
D Diabetes 1
S2 Prior Stroke, TIA or thromboembolism 2
V Vascular disease (including ischaemic heart disease and peripheral arterial disease) 1
S Sex (female) 1

0 No treatment
1 Males: Consider anticoagulation
Females: No treatment (this is because their score of 1 is only reached due to their gender)
2 or more Offer anticoagulation

If CHADVASc = 0, TTE to exclude valvular disease (+Afib = absolute indication for anticoag)

21
Q

AFib: anticoagulation

A

1st line: DOAC (apixaban, dabigatran, edoxaban, rivaroxaban)
2nd line: warfarin

DOAC>warfarin = no regular INR checks

NO ASPIRIN

22
Q

Rate vs rhythm control in Af (haemodynamically stable patients)

A

< 48 hours: rate or rhythm control
≥ 48 hours or uncertain (e.g. patient not sure when symptoms started): rate control
if considered for long‑term rhythm control, delay cardioversion until they have been maintained on therapeutic anticoagulation for a minimum of 3 weeks

23
Q

Afib: rate control agents

A

beta-blockers
dronedarone: second-line in patients following cardioversion
amiodarone: particularly if coexisting heart failure

24
Q

Afib: indication for catheter ablation

A

Patients with AF who have not responded to or wish to avoid, antiarrhythmic medication

25
Catheter ablation: technical aspects
Objective: ablate the faulty electrical pathways that are resulting in atrial fibrillation. This is typically due to aberrant electrical activity between the pulmonary veins and left atrium percutaneously, typically via femoral vein both radiofrequency (uses heat generated from medium frequency alternating current) and cryotherapy can be used to ablate the tissue
25
Catheter ablation: technical aspects
Objective: ablate the faulty electrical pathways that are resulting in atrial fibrillation. This is typically due to aberrant electrical activity between the pulmonary veins and left atrium percutaneously, typically via femoral vein
26
Catheter ablation: anticoagulation
- 4 weeks before and during the procedure - patients still require anticoagulation as per their CHA2DS2-VASc score if score = 0: 2 months anticoagulation recommended if score > 1: longterm anticoagulation recommended
27
Catheter ablation: COMPLICATIONS
cardiac tamponade stroke pulmonary vein stenosis
28
Catheter ablation: success rate
around 50% --> early recurrence (within 3 months) of AF that often resolves spontaneously longer term, after 3 years, around 55% of patients who've had a single procedure remain in sinus rhythm. multiple procedures --> around 80% are in sinus rhythm
29
Afib: post-stroke
- following a TIA, anticoagulation for AF should start immediately (once imaging excludes haemorrhage) - in acute stroke patients, in the absence of haemorrhage, anticoagulation therapy should be commenced after 2 weeks
30
Afib: Electrical cardioversion
Synchronised to R wave
31
Afib: pharmacological cardioversion
<48hrs Amiodarone or flecainide
32
Cardioversion: anticoagulation
AF for more than 48 hours then anticoagulation should be given for at least 3 weeks prior to cardioversion. Following electrical cardioversion if AF is confirmed as being less than 48 hours duration then further anticoagulation is unnecessary
33
AVNRT
Small circuit around AV nodal tissue - Re-entrant within AV node - Fast and regular - ECG: regular narrow complex tachycardia
34
AVRT
- Pre-excitation: in V1, initial slurring of QRS (delta wave) with short PR - Accessory pathway that allows electrical activation from atria to the ventricle (in addition to usual conduction down AV node) Orthodromic AVRT -> ventricle activated down his-purk, circuit completed by going up into atria by bundle of Kent Antidromic AVRT: ventricles activated by the accessory pathway, hence R ventricle before left -> broad QRS tachycardia
35
Wolf-Parkinson White (AVRT) - ECG - Types - Associations - Management
congenital accessory conducting pathway between the atria and ventricles leading to a atrioventricular re-entry tachycardia (AVRT) ECG - short PR interval - wide QRS complexes with a slurred upstroke - 'delta wave' Axis deviation - left axis deviation if right-sided accessory pathway (Most common) - right axis deviation if left-sided accessory pathway Types type A (left-sided pathway): dominant R wave in V1 type B (right-sided pathway): no dominant R wave in V1 (most common) Associations HOCM mitral valve prolapse Ebstein's anomaly thyrotoxicosis secundum ASD Management definitive treatment: radiofrequency ablation of the accessory pathway medical therapy: sotalol***, amiodarone, flecainide ***sotalol should be avoided if there is coexistent atrial fibrillation as prolonging the refractory period at the AV node may increase the rate of transmission through the accessory pathway, increasing the ventricular rate and potentially deteriorating into ventricular fibrillation
36
Bradycardia: life-threatening signs
Same as tachycardia - Shock - Myocardial ischaemia - Syncope - Heart failure
37
Bradycardia: life-threatening signs present
Atropine 500mcg
38
Bradycardia: life-threatening signs not present
Risk of asystole? * Recent asystole * Mobitz II AV block * Complete heart block with broad QRS * Ventricular pause > 3 s
39
Bradycardia: life-threatening signs not present + no risk of asystole
Observe
40
Bradycardia: (life-threatening signs not present AND risk of asystole) OR Unsatisfactory response to Atropine
Interim measures: * Atropine 500 mcg IV repeat to maximum of 3 mg * Isoprenaline 5 mcg min-1 IV * Adrenaline 2–10 mcg min-1 IV * Alternative drugs* or Transcutaneous pacing
41
If interim measures do not work
Seek expert help --> arrange transvenous pacing
42
What is the MoA of atropine?
Blocks parasympathetic innervation
43
Cautions and contra-indications to the use of Adenosine
CIs - central line access or - If already on dipyridamole or carbamazepine. - Asthma (use verapamil instead) Adenosine may be used in patients with heart transplants for rapid reversion to sinus rhythm and to aid the diagnoses of broad/narrow complex supraventricular tachycardias. It is important to note that patients with heart transplants are very sensitive to the effects of adenosine.
44
List complications of SVT
Syncope Deep vein thrombosis Embolism Cardiac tamponade Congestive cardiac failure Myocardial infarction Death
45
What are the 3 broad categories of device therapy
1. For Bradycardia o Pacemaker – ensures HR never drops below certain value 2. Susceptible to VT/VF (previous event or yet to have but have high risk) o Implantable Cardioverter Defibrillator (ICD) – shocks heart if it finds VT/VF 3. Cardiac resynchronisation o BiVentricular (BiV) /Cardiac Resynchronisation Therapy (CRT) devices – placed to pace heart at all times in specific manner so that R and L ventricles contract simultaneously
46
List causes of bradycardia
Can be normal in athletic individuals Electrolyte disturbances Hypothyrodism Myocardial Infarction Sepsis Drugs e.g beta blockers Increased intracranial pressure Heart block