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Cardio > ECG: Tachycardia > Flashcards

ECG: Tachycardia Flashcards

1
Q

A patient has tachycardia with a narrow QRS complex. Rhythm is irregular. What are your differentials?

A
  • Atrial fibrillation,
  • multifocal atrial tachycardia
  • atrial flutter with variable conduction
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2
Q

A patient has tachycardia with a narrow QRS complex. Rhythm is regular. What are your differentials?

A
  • atrial flutter,
  • sinus tachycardia,
  • AVNRT, AVRT
  • atrial tachycardia
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3
Q

A patient has tachycardia with a broad QRS complex. Rhythm is regular. What are your differentials?

A
  • Ventricular tachycardia
  • Supraventricular tachycardia with abberancy e.g. WPW or BBB
  • SVT with pre-excitation
  • antidromic avrt
  • pre excited SVT
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4
Q

A patient has tachycardia with a broad QRS complex. Rhythm is irregular. What are your differentials?

A
  • atrial fibrillation with abberancy
  • pre- excited AF
  • atrial flutter with aberrancy and variable conduction
  • polymorphic vt
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5
Q

What are pathological causes of sinus tachycardia?

A

Pathological causes: congestive cardiac failure, severe lung disease, sepsis, hyperthyroidism, pulmonary embolism

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6
Q

How does junctional escape rhythm present?

A
  • When AV Node becomes the pacemaker! W/ regular rate of 40-60bpm
  • Narrow QRS complexes
  • No relationship between the QRS complexes and any preceding atrial activity (e.g. P-waves, flutter waves, fibrillatory waves)

P waves may be present / absent; if present:

  • Can appear before, during, or after QRS
  • Are usually inverted (retrograde) in inferior leads, and +ve in aVR, V1
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7
Q

How does premature atrial contraction (PAC) present?

A

P wave of premature beat is different from sinus P in Morphology & axis

  • The abnormal P wave may be hidden in the preceding T wave 🡪 “peaked” or “camel hump” appearance
  • PACS arising close to the AV node activate the atria retrogradely, producing an inverted P wave with a relatively short PR interval ≥ 120 ms

Regular rhythm

Timing – P wave comes too early

A non (fully) compensatory pause

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8
Q

What is the morphology of premature junctional contraction?

A
  • Originates near AV node hence absent or retrograde P wave

- A (fully) compensatory pause

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9
Q

What are the symptoms of paroxysmal supraventricular tachycardia?

A

palpitations, dyspnoea, dizziness, syncope

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10
Q

What are the triggers of paroxysmal supraventricular tachycardia?

A

A Fib, PAC

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11
Q

What are the relieving factors of paroxysmal supraventricular tachycardia?

A

increased vagal tone from Carotid Massage / Valsava helps ABORT
Management

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12
Q

What are the characteristics of AVNRT on ECG?

A

• Narrow QRS complex
• HR 130-250/min
• Wide QRS Complex AVNRT possible if there is a pre existing BBB / rate aberrant conduction
• Atrial conduction occurs retrogradely producing inverted P waves in inferior leads (II, III, aVF)
• Atrial and ventricular depolarisation occur simultaneously – P waves frequently buried in QRS complex
• P wave may ‘distort’ last part of QRS complex
- Pseudo S wave in inferior leads
•- Pseudo R wave in V1
• Can try vagal manoeuvres first, after which can try adenosine 6,12,12mg

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13
Q

What are the characteristics of pre-excitation AVRT on ECG?

A
  • short PR interval

- PR segment cannot be seen in some cases

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14
Q

What are the characteristics of orthodromic AVRT on ECG?

A

Anterograde conduction through AV node

  • Narrow complex QRS tachycardia due to fast conduction via bundle of His
  • There is no more upstroke because the accessory bundle will always be in refractory
  • Retrograde P waves after QRS
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15
Q

What are the characteristics of antidromic AVRT on ECG?

A

Retrograde conduction through AV node

  • There is wide complex QRS tachycardia because the ventricles are depolarised via excitation that reaches via the accessory bundle
  • P waves RARELY seen (because of widened QRS 🡪 P waves tend to be buried within T waves)
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16
Q

What is the morphology of WPW with A fib?
• Atrial fibrillation can occur in up to 20% of patients with WPW
• Accessory pathway allows for rapid conduction directly to ventricles bypassing the AV node
• Rapid ventricular rates may result in degeneration to VT or VF

A

• Rate > 200 bpm
• Irregular rhythm
• Wide QRS complexes due to abnormal ventricular depolarisation via
accessory pathway
• Axis remains stable unlike Polymorphic VT

17
Q

What is the management of WPW with A fib?

A
  • AV node is rate-limited, hence despite hundreds of bpm of atria in A Fib, ventricles depolarise at a max of 200bpm
  • In pt w BOK & A Fib, direct depolarisation of ventricles in can lead to Ventricular Fibrillation -> SUDDEN CARDIAC DEATH!
  • HOWEVER, in most of these pts majority of A Fib impulses travel thru AV node instead! Hence does not lead to Sudden Cardiac Death!
  • However, we CANNOT give AV nodal blocking agent to treat A Fib in these pt -> will force signal down BOK -> V Fib -> death
  • Hence, BB, CCB, Amiodarone and Digoxin are C/I
  • Instead, we opt to use Procainamide which selectively blocks the accessory pathway conduction
18
Q

What are the features of atrial flutter on ecg?

A
  • Narrow complex tachycardia
  • Regular atrial activity (≈300bpm)
  • Loss of isoelectric baseline
  • Flutter waves (saw-tooth pattern) best seen in leads II, III, AVF
  • Saw-tooth waves have a fast upslope and slow downslope
  • Fixed (e.g. 2:1, 3:1) or variable AV blocks

Variations

  • May have variable block resulting in irregular rhythm mimicking AF
  • 1:1 conduction may occur in sympathetic stimulation or in WPW

Most common: counter-clockwise –> Flutter waves negative in leads II, III, aVF and positive in V1

19
Q

What is the management of atrial flutter?

A

Carotid massage may increase degree of block (e.g. 2:1 to 4:1), making it easier to visualize

Treatment

  • Hemodynamically unstable – electrical cardioversion
  • Rate control (beta blocker, CCB)
  • Rhythm control (amiodarone)
  • Anticoagulation
  • Cavotricuspid isthmus ablation
20
Q

What are the features of atrial fibrillation on ecg?

A
  • Irregularly irregular rhythm
  • Chronic, fibrillatory waves
  • No P waves (atrial rate 350-500)
  • Absence of an isoelectric baseline
  • Variable ventricular rate
  • Complications of AF include hemodynamic instability, cardiomyopathy, cardiac failure, and embolic events
21
Q

What are the causes of atrial fibrillation?

A

Common

  • cardiac: advanced age, hypertension (most common), ischaemic heart disease, valvular heart disease, heart failure
  • non cardiac: thyrotoxicosis, sepsis/ acute stress, electrolyte disturbances

Less common

  • cardiac: myocarditis/ pericarditis, post cardiac surgery
  • non cardiac: obstructive sleep apnea COPD with cor pulmonale, drugs (theophylline/ illicit drugs, long term amiodarone)
22
Q

What is the management of atrial fibrillation?

A

Investigate: 2D echocardiogram

Rate control – Target <110bpm

  • Amiodarone: Mainly rhythm control; but also slows down rate. May be used in acute setting if you don’t know if there is structural heart disease or not
  • Beta blocker 🡪 1st line (especially for patients with HF)
  • Calcium channel blockers (non-dihydropyridines) if beta blockers contraindicated
  • Digoxin (hardly used)

Rhythm control

  • Management dependent on patient profile, symptoms
  • Pharmacological: Class IC, III agents
  • Electrical cardioversion

Anticoagulation

  • CHADSVASC2 score ≥2 & HASBLED score
  • Warfarin vs NOACs (Dabigatran, rivaroxaban, apixaban)
23
Q

What is the ecg findings found in multifocal atrial tachycardia?

A
  • Heart rate usually 100-150bpm
  • Irregularly irregular rhythm with varying PP, PR and RR intervals
  • At least 3 distinct P wave morphologies in same lead
  • Isoelectric baseline between P waves (i.e. no flutter waves)
  • Absence of single dominant pacemaker (i.e. not sinus rhythm with frequent PACs)
  • Usually occurs in patients with underlying respiratory failure (e.g. COPD exacerbation, decompensated heart failure)
24
Q

What is the ecg findings found in paroxysmal atrial tachycardia?

A

Single foci: either enhanced automaticity or re-entrant circuit

Regular, Rate 100-200 bpm

Each QRS preceded by abnormal P wave (upright in V1, negative in II, III, AVF)

May be difficult to differentiate from PSVT; but look for:

  • Warm up (irregular period) & cool down (termination) period in automatic form
  • Carotid massage no effect in PAT
25
Q

What are the ecg features of torsades de pointes

A
  • Specific form of polymorphic VT
  • Characteristic morphology: QRS complexes “twist” around isoelectric line
  • Occurs in context of QT prolongation
  • Usually initiated by a VPB starting at the peak of a prolonged T-U wave (“R on T” phenomenon)
26
Q

What are the features of WPW syndrome?

A
  • PR interval <120ms
  • Delta wave – slurring slow rise of initial portion of the QRS
  • QRS prolongation >110ms
27
Q

What are features suggestive of VT?

A
  • AV dissociation
  • Capture beats
  • Fusion beats
  • North-west axis
  • Broad QRS complexes
  • Negative concordance
28
Q

What are the ecg features of AF with complete heart block?

A
  • Fibrillatory baseline, absence of P waves
  • Slow rate of 50
  • R-R intervals regular
  • QRS narrow suggestive of supra-Hisian escape rhythm

Cardio (16 decks)

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