Tachyarrythmia

Question 1

Narrow complex tachyarrythmia classification

Answer 1

• HR >100
• QRS <0.12ms
• Absent or abnormal P-waves

Question 2

Examples of narrow complex tacharrythmias

Answer 2

AF
Atrial flutter
SVT
Sinus tach

Question 3

Wide complex tacharrythmia classifcation

Answer 3

• HR >100
• QRS >0.12ms
• Wide and bizzare
• AV dissociation/loss of p-waves

Question 4

Examples of wide complex tacharrythmias

Answer 4

VT

Question 5

AVNRT definition

Answer 5

Atrial tachycardia caused by a re-entry circuit within the AV node (DOES NOT use an accessory pathway).

Question 6

AVNRT pathophysiology

Answer 6

A premature beat occurs, slow pathway is not in a refractory period.
Impulse is sent down the slow pathway which also activates the fast pathway because by the time it reaches the fast pathway, fast not in refractory period.
The signal continues along the fast pathway, activating the slow pathway again and loop is continued.
This sends signal to ventirciles at a faster rate.

Question 7

AVRT definition

Answer 7

Atrial tachycardia is associated with a re-entry circuit utilising an accessory pathway to the AV node. Most common bundle of kent.

Question 8

SVT vs. VT

Answer 8

• VT with aberrancy (wide QRS) can look suspiciously like VT
• the best way to tell the difference is the haemodynamic stability of the patient; a patient in SVT will usually have a better BP and HR than someone in conscious VT
• SVT often occurs in younger patients, thus if the patient is >35 years of age, there is an 80% chance it is VT
• previous history of MI also significantly increases the chance that is it VT
• roughly, VT tends to be 140-160bpm
• SVT roughly sits between 180-240bpm, however, rate alone should NOT be a diagnostic tool

Question 9

SVT characteristics and clinical presentation

Answer 9

• The rate of SVT will be fixed and regular, even with activity, and in paediatrics is generally >220 bpm with a narrow complex QRS.
• P-waves are either absent or after the QRS complex because there is no conduction from the SA node
• The clinical presentation of SVT can include palpitations, chest pain, shortness of breath, lethargy, feeding difficulties, irritability, dizziness and occasional loss of consciousness due to a decreased cardiac output resulting in cardiogenic shock

Question 10

SVT Management - hemodynamically stable

Answer 10

Modified valsalva manoeuvre:
1. Ensure a complete set of vital signs are established.
2. Reassure the patient and explain the procedure.
3. Suitably position the monitor so that it can be viewed by the paramedics.
4. The patient should remain in a Semi-recumbent position
5. Give the patient a new 10mls syringe and ensure the barrel/plunger are able to freely moved
8. Whilst holding the syringe tip firmly by the lips, have the patient exhale forcefully pushing the syringe plunger outward for
approximately 15 seconds.
9. At the end of the forced exhalation immediately position the patient supine with legs raised straight for 15 seconds. .
10. Reposition the patient to the semi-recumbant position for 45 seconds
11. Note any changes on the Monitor and record the 12 lead ECG
12. Confirm the SVT has reverted.
13. Consider repeating the procedure for a maximum of 3 attempts should the SVT not revert

Question 11

Contraindications to modified Valsalva

Answer 11

• Hemodynamically unstable patient (SBP <90mmHg)
• AF/flutter
• AMI
• Third trimester pregnancy
• Coronary artery stenosis

Question 12

Complications of modified valsava

Answer 12

Prolonged hypotension
Syncope

Question 13

Describe the four phases that occur during modified valslva

Answer 13

1. Phase one – a transient increase in aortic pressure and a compensatory decrease in heart rate, due to increased intrathoracic pressure generated during forced exhalation against resistance.
2. Phase two – the end of the transient period, with a decrease in aortic pressure as a consequence of reduced venous return and hence cardiac output, with baroreceptor response leading to increased heart rate.
3. Phase three – the end of the strain phase of the Valsalva manoeuvre, with further decrease in aortic pressure and compensatory rise in heart rate.
4. Phase four – increased venous return accentuated by raising legs leading to increasing aortic pressure and compensatory decrease in heart rate, with subsequent return to resting heart rate.

Question 14

SVT management - hemodynamically unstable

Answer 14

1. Adenosine 6mg; after 2 mins if no response; 12 mg (repeated if no response after 2 mins)
2. Synchronised cardioversion