Tachydysrhythmias Flashcards

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1
Q

What is tachycardia?

A

Resting heart rate of > 100 bpm in adults

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2
Q

General Approach to tachycardia: Is the patient stable or unstable?

A
  1. Monitor in high acuity area with continuous cardiac and vitals monitoring
  2. Assess responsiveness and pulse. If pulseless, begin CPR
  3. ABCs, set IV plug
  4. Assess for clinical features of UNSTABLE patient: Chest pain, Hypotension, AMS, Pulmonary edema, Shock (CHAPS)
  5. 12 lead ECG if patient is stable
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3
Q

Ddx for:
Narrow, regular complex tachycardia

A
  1. Sinus tachycardia
  2. Supraventricular tachycardia
  3. Atrial flutter with fixed conduction
  4. Atrial tachycardia
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4
Q

Ddx for:
Narrow, irregular complex tachycardia

A
  1. Atrial fibrillation (**most common)
  2. Atrial flutter with varying conduction
  3. Multifocal atrial tachycardia
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5
Q

Ddx for:
Wide, regular complex tachycardia

A
  1. Monomorphic ventricular tachycardia
  2. Metabolic/Drug
  3. SVT with antidromic conduction through an accessory pathway
  4. SVT with abberancy/bundle branch block
  5. Any narrow, regular tachycardia with a bundle branch block
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6
Q

Pathophysiology of Atrial Flutter

A

An atrial re-entrant rhythm that overrides the sinus node leading to atrial depolarisation at a rate of 300/min as seen as flutter waves in ECG resulting in saw toothed baseline.

Due AV nodal refractory period, conduction to the ventricles (ventricular depolarisation) occurs at regular intervals in 2:1 or 3:1 ratio, resulting in a ventricular rate of 150 or 100 beats per minute.

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7
Q

Sinus tachycardia: Key Features

A
  1. Narrow, regular complex tachycardia
  2. Normal-looking P wave before every QRS complex
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8
Q

Sinus tachycardia: Causes

A
  • Physiological e.g. exercise, infection, pyrexia, dehydration
  • Emotional: Pain, Anxiety
  • Emergencies: acidosis, pulmonary embolism, cardiac tamponade, significant bleeding with hypovolaemia
  • Hyperthyroidism
  • Medications
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9
Q

Sinus tachycardia: Treatment

A

Treat underlying cause

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10
Q

Atrial Flutter: Key Features

A

*narrow, regular or irregular complex tachycardia

  1. Saw toothed baseline flutter waves in some of the leads
  2. Lack of TP segment in the leads with a saw toothed pattern
  3. Ventricular rate typically about 100 or 150 bpm
  4. Rhythm is regular in cases with fixed conduction ratio
  5. If the conduction ratio varies, then the rhythm is irregular
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11
Q

Pathophysiology of Atrial Fibrillation

A

Many ectopic atrial foci depolarising almost simultaneously (fibrillating), hence ventricular depolarisation occurs irregularly.

  • Reentrant Circuits: The disorganized impulses lead to the formation of reentrant circuits within the atria. These circuits continuously stimulate different parts of the atrial myocardium, causing the atria to fibrillate (quiver) rather than contract effectively.
  • Impaired Conduction: The rapid, irregular impulses overwhelm the atrioventricular (AV) node, which tries to regulate the transmission of impulses to the ventricles but often cannot keep up. This results in an irregular ventricular response rate.
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12
Q

Atrial Fibrillation: Key Features

A
  1. Irregularly irregular rhythm
  2. Fine or coarse fibrillatory waves may be present. Coarse waves may mimic P waves
  3. Absence of P waves before every QRS complex
  4. Absence of isoelectric baseline
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13
Q

Atrial Flutter/Fibrillation: Treatment

A
  1. Treat reversible causes - infection, AMI, thyrotoxicosis, alcohol, acute PE, myocarditis
  2. Rate control
    a. No HF
    - Diltiazem
    - Verapamil
    - Esmolol
    - Metoprolol
    - Procainamide
    b. HFpEF
    - CCB or BB
    c. HFrEF
    - Amiodarone
    - Digoxin
  3. Start anticoagulants if patient’s CHA2DS2VASc is 2 or more
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14
Q

CHA2DS2VASc score

A

Congestive heart failure
Hypertension
Age >/= 75 years
Diabetes mellitus
Stroke/TIA/thromboembolism
Vascular disease (prior MI, PAD, aortic plaque)
Age 65-74years
Sex category: Female

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15
Q

Supraventricular tachycardia

A

It refers to all atrioventricular tachydysrhythmias that occurs above the ventricles (Bundle of His) and the types of SVT depends on the source of the electrical signal
- AVNRT, AVRT, atrial flutter/fibrillation, atrial tachycardia

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16
Q

Most common cause of SVT

A

Atrioventricular nodal re-entrant tachycardia

17
Q

Pathophysiology of AVNRT

A

Re-entrant circuit is formed
Re-entry point of electrical impulse is back through the AV node and into the atria again

18
Q

Pathophysiology of AVRT

A

Re-entrant circuit is formed
Re-entry point of electrical impulse is through an accessory pathway (additional electrical pathway between atrium and ventricle)
- Conduction can be orthodromic or antidromic

19
Q

Orthodromic AVRT

A

Conduction of electrical impulse is from atrium to ventricles through AV node and then some impulses will reenter the atrium through the accessory pathway

20
Q

Antidromic AVRT

A

Conduction of some electrical impulse goes from atrium to ventricles through the accessory pathway then will reenter the atrium through AV node

21
Q

SVT: Key features

A
  1. Narrow, regular complex tachycardia
  2. Absence of P wave before every QRS complex
22
Q

Stable SVT: Treatment

A
  1. Non-pharmacological manoeuvre
    - Modified valsava manoeuvre
    - Carotid sinus massage
  2. Pharmacological treatment
    - IV adenosine*
    - IV diltiazem
    - IV verapamil
23
Q

Unstable SVT: Treatment

A

Synchronised electrical cardioversion

24
Q

Unstable Atrial flutter/Afib: Treatment

A

Synchronised cardioversion
- Atrial flutter: 50J
- Atrial fibrillation: 100J

25
Q

Ventricular tachycardia

A

A regular, wide complex tachycardia that is sustained for >/= 30 seconds
- QRS complex > 120ms wide
- Rate > 120bpm

26
Q

Ventricular tachycardia: Key features

A

CABAM

Concordance
- When all the precordial leads point in the same direction

Axis
- Northwest Axis
- QRS positive in aVR
- Negative in I and aVF

Beats: Fusion and capture beats

AV dissociation
- A and V don’t talk
*most common feature

Morphology
- Deviations from normal BBB morphology suggests VT

27
Q

Stable ventricular tachycardia: Treatment

A
  • IV amiodarone
  • IV lignocaine
  • IV procainamide
  • If pharmaco fails: elective synchronised cardioversion (in ED if unstable)
28
Q

Pulseless VT: Treatment

A

Start CPR (ACLS)

29
Q

Torsades de pointes: Treatment

A
  1. Correct electrolyte abnormalities causing prolonged QT especially hypoMg and hypoK.
  2. IV MgSO4 1-2g over 60-90s then 1-2g/h infusion.
  3. Consider overdrive pacing under the care of a cardiologist.
  4. Halt any drugs which may cause QT prolongation. (Eg. Procainamide, amiodarone, sotalol, TCAs, macrolides.)
30
Q

Polymorphic VT: Treatment

A
  1. Amiodarone for chemical cardioversion.
  2. Look for evidence of ischemia.
  3. Look out for QTc>500ms or ‘R on T’ phenomenon suggesting impending TdP development.