ECG

Question 1

Pre-excitation syndrome

Answer 1

WPW in sinus rhythm
• PR interval < 120 ms
• Delta wave- slurring of initial portion of QRS
• QRS duration > 110 ms
• Supporting
○ Secondary ST/T wave repolarisation (abnormal depolarisation causes abnormal repolarisation)
§ ST segment and T wave changes are discordant to QRS direction

	* Type A has a positive delta wave in all precordial leads with R/S > 1 in V1
	* Type B has a negative delta wave in leads V1and V2

AVRT with orthodromic conduction
	○ Rate 200 - 300
		§ (too fast for sinus rhythm. Sinus tachy max rate = 220 - age)
	○ P wave may be buried in QRS complex or retrograde
	○ QRS width < 120 ms- unless pre-existing bundle branch block or aberrant conduction
	○ QRS alternans
		§ phasic variation in QRS amplitude associated with AVNRT and AVRT, distinguished fromelectrical alternansby a normal QRS amplitude

	○ "Pseudoischemia"
		§ ST depression and TWI common, does not signify ischemia

		Treatment

			□ Haemodynamically unstable (hypotension, altered mental state, APO)
				® Urgent synchronised DC cardioversion
			□ Haemodynamically stable --> Treat like PSVT
				® Vagal manoeuvre
				® Adenosine or calcium Ch blocker
				® DC cardioversion if unresponsive to medical therapy

AVRT with antidromic conduction
	○ Less common, only 5% of WPW
	○ Rate 200 - 300
		§ (too fast for sinus rhythm. Sinus tachy max rate = 220 - age)
	○ Wide QRS complex (due to abnormal ventricular depolarisation via accessory pathway)
	○ Can be confused with VT
		§ differentiating VT from SVT with aberrancy.

		Treatment
			□ Haemodynamically unstable (hypotension, altered mental state, APO)
				® Urgent synchronised DC cardioversion
			□ Haemodynamically stable --> treat like broad complex tachy
				® Amiodarone
				® Procainamide
				® Ibutilide
				DC cardioversion if unresponsive to medical therapy

AF / Aflut with WPW
	○ Rate > 200, usually 300 - 600
	○ "Irregular, broad complex, polymorphic tachy, without turning off the point"

	Treatment
		• Haemodynamically unstable (hypotension, altered mental state, APO)
			○ Urgent synchronised DC cardioversion
		• Haemodynamically stable --> treat like broad complex tachy
			○ Never AV nodal blocking agent (adenosine, Ca Ch blocker, beta blocker) --> can increase conduction through accessory pathway --> can degenerate to VT or VF
			○ Procainamide or Ibutilide
			○ DC cardioversion if unresponsive to medical therapy

Question 2

Blocks

Answer 2

• LAFB
□ LAD
□ QRS <120 ms
□ Exclude other causes of LAD (LVH, inferior MI, ventricular ectopic, paced rhythm)
□ Supporting
® R wave peak time in aVL > 45ms
® qR in lateral leads (I, aVL), rS in inferior leads (II, III, aVF)

		• LPFB
			□ RAD >90 deg
			□ QRS <120 ms
			□ Exclude other causes of RAD (RVH, lateral MI, ventricular ectopic, RV strain from PE or COPD, TCA overdose)

			Supporting
				® R wave peak time in aVF >45 ms
				® rS in I and aVL
				® qR in II, III, and aVF

		• Bifascicular block
			□ RBBB + LAFB or LPFB (= RBBB + LAD or RAD)
			□ Signifies extensive conducting system disease, but low risk (<1%/yr) to progress to complete heart block

		• Trifascicular block
			□ Incomplete trifascicular block
				® Bifascicular block + 1st or 2nd degree AV block
				® Bifascicular block + alternating LAFB (LAD) and LPFB (RAD)
				--> can progress to CHB although low risk. Syncope + incomplete trifascicular block = admit under telemetry, ?episodes of CHB ?need PPM.
			□ Complete trifascicular block Bifascicular block + 3rd degree AV block

Question 3

Hypertrophy

Answer 3

I try to do this stupid thing