SVT - Supraventricular Tachycardia

Question 1

What is the normal electrical activity of the heart?

Answer 1

1) Starts in SA node and travels through the R and L atrium causing atrial contraction
2) The impulse then travels through the AV node, which delays the impulse to allow for ventricular filling before relaying to the Bundle of His -> Purkinje fibres first towards the apex and then back towards the annulus fibrosus (outside)

This occurs in one direction (foreshadowing to SVT)

Question 2

Where does the SA node lie?

Answer 2

Right atrium

Question 3

Define SVT

What is the pathophysiology of SVT

Answer 3

Tachycardia (broad or narrow complex) originating from above the His-Purkinje system

In SVT, The electrical pathway does not occur in one direction and hence the electrical signal, originating from above the His-Purkinje system, re-enters the atria creating a self-prepetuating electrical loop.

Question 4

List the 5 types of SVT

Answer 4

Main:
1) AV nodal re-entrant tachycardia
2) AV re-entrant tachycardia
3) Atrial tachycardia
Other:
4) MAT - Multifocal atrial tachycardia
5) SANRT - SA nodal re-entrant tachycardia

Note: The others have different pathophysiology but same tx

Question 5

SVT may be persistent or paroxysmal (intermittent). How does a broad complex SVT occur?

Answer 5

If there is SVT + Bundle branch block -> Broad complex tachycardia

If just SVT, it is narrow complex

Question 6

List the 3 main types of SVT along with a brief definition/description of what each is.

Answer 6

1) AV nodal re-entrant tachycardia
Re-entry within or near the AV node

2) AV re-entrant tachycardia
Accessory pathway causing re-entry

3) Atrial tachycardia
Electrical signal is generated by an ectopic source within the atria

Question 7

The AV node has 2 pathways. What are these pathways?
Then explain them in the context of AV nodal re-entrant tachycardia

Answer 7

Fast pathway: Fast conduction, long refractory period
Slow pathway: Slow conduction but shorter refractory period

So what happens here is that the fast pathway is still refractory. When an early electrical impulse from the atria meets the refractory fast pathway, it is not ready to conduct it => the impulse travels down the slow pathway instead.

By the time this impulse reaches the common pathway (between the slow and fast), the impulse travels backwards (retrograde) back up the fast pathway => creating a loop of sustained tachycardia

Question 8

What is meant by the term sinus tachycardia

Answer 8

Means everything is normal including the presence of all components except the fact that the rate is >100bpm

Question 9

How would an ECG of typical SVT look like?

Answer 9

Regular Tachycardia + Absent P waves (embedded or inverted in inferior leads), Narrow QRS <80

Question 10

what is the normal PR, QRS, and QT intervals

Answer 10

PR - 120-200ms/0.12-0.2s
QRS - 80-100/120ms
QT - 350-450ms

Question 11

Which pathway is associated with WPW?

Explain WPW showing me:
Honours - Name of 2 types of arrhythmias?
Name of accessory pathway?
How does WPW appear on ECG?

Answer 11

AV re-entrant tachycardia (AVRT)
Wolf-parkinson-white syndrome is characterized by a orthodromic (narrow complex) or antidromic (broad complex) pathway that travels via an accessory pathway called the Bundle of Kent

ECG:
Short PR interval <120ms
Slurred upstroke delta waves
Widened QRS complex >100ms

Question 12

What is significant about the epidemiology of SVT?

Answer 12

F>M
It is a common tachycardia in young females

Question 13

You are taking a cardiac history and want to cover symptoms related to an arrhythmia. What are the symptoms of SVT (which are common with every arrythmia) should you ask about within the history.

Answer 13

Palpitations
Syncope/pre-syncope
SOB/Dyspnoea
Chest pain
Fatigue
! feeling of rapid neck pulsation !

Question 14

How does an arrhythmia cause SOB/dyspnoea and chest pain?

Answer 14

Reduced cardiac output + coronary artery hypo-perfusion

Explanation:
Diastolic flow is required for coronary perfusion
In Tachyarrhythmias, there is not enough time for diastolic flow to sufficiently perfuse the coronary arteries

In Bradyarrhythmias Cardiac output is not sufficient to allow for sufficient perfusion

Question 15

What is Long QT syndrome
What can it lead to?

Answer 15

It is a genetic (literally LQT1,2,3) or acquired syndrome characterized by a long QT on ECG which can cuase life-threatening arrhythmias such as Torsades De Points

Question 16

What medications may cause long QT syndrome?

Answer 16

Class Ia and III antiarrhythmics (Quinidine, procainamide/ amiodarone, sotalol, ibutilide)

Antibiotics: Macrolides (azithromycin, clarithromycin, erythromycin)
Fluoroquinolones (ciprofloxacin, levofloxacin)

Antifungals (azoles)

Antidepressants: both typical and atypical

Antipsychotics: TCAs, SSRIs

Antiemetics: ondansetron (5HT-3 receptor antagonist)

Methadone (opioid)

Question 17

Briefly, what is Torsades de Points?

Answer 17

It is a type of ventricular tachycardia whereby QRS complexes appear to rotate around the baseline

Question 18

List the RFs for SVTs

Answer 18

Modifiable:
Drugs: Nicotine, alcohol, cocaine
Acquired LQT (medications)
Hyperthyroidism

Non-modifiable:
Family history of sudden cardiac death
Previous cardiac surgery
LV dysfunction (HF)
Genetic Long QT syndrome (LQT1,2,3)

Question 19

What are the signs of SVT?

Answer 19

Vitals: HR>100, BP normal or low
Diaphoretic, distressed on general inspection
Scars such as previous CABG or stenting is a RF
Visible rapid pulsation in the neck

Question 20

What investigations will you carry out for an SVT

Answer 20

As for any arrhythmia: except ECG
Bedside:
ECG/!Holter monitor: Looking for Regular Tachycardia + Absent P waves (embedded or inverted in inferior leads), Narrow QRS <80 + screen for previous MI, BBB, or LV
Urine dipstick (sepsis)
Urinalysis (evidence of CKD to guide management between DOAC and Warfarin) + Toxicology

Bloods:
FBC - Anaemia, infection, low platelets if DIC, infection, sepsis)
CRP - raised in infl. + inf.
U&E - Hypomagnesia + hyper/hypokalaemia + medications
TFTs - hyperthyroidism
Troponin + CKMB (ischaemia as a cause or result of arrhythmia)
BNP - HF in severe arrhythmia
HbA1c and Lipid profile (RFs)

Imaging:
CXR - sx of HF (ABCDE)
ECHO - TTE - atrial/ventricular size (LA enlargement/LV hypertrophy), RV systolic pressure, valvular involvement, pericardial disease - TOE - LA (appendage) thrombus, Rule out vegetations in IE

Procedure: Exercise stress test - helps identify ischaemia (not rly done so not required for 5/5)

Question 21

How would you manage an acute narrow complex tachycardia (SVT)

Answer 21

Notice how I phrased the question for MCQs. This can be life threatening so it is treated as an emergency

First I will perform ABCDE, take bloods, and perform continuous ECG monitoring to determine if the patient is stable or unstable/life-threatening features.

Then I will place
Remember that these sometimes occur alongside other diseases such as MI or sepsis

If unstable -> urgent synchronised cardioversion

If stable ->
1) Valsalva manouvre
2) Carotid sinus massage
3) Adenosine 6mg IV followed by saline flush -> 12mg -> 18mg
4) Non-dihydro CCB. (class 4) + Beta blockers (class 2)
IV Verapamil 5-10mg -> +10mg if ineffective after 30 mins -> + Metoprolol
5) Synchronised cardioversion

THIS IS THE ONLY TIME BETA BLOCKERS AND NON-DIHYDRO CCB ARE EVER COMBINED => caution for severe bradycardia and hypotension

Question 22

How is the valsalva manouvre performed?

Answer 22

Patient blows into a syringe to blow plunger away

Question 23

Briefly explain what a carotid sinus massage is and how it is performed

Answer 23

Carotid sinus massage is a clinical manouvre used to help terminate SVT by sitmulating the carotd sinus which is a baroreceptor => increasing vagal tone with increased pressure from the massage

First must exclude carotid stenosis via duplex US and carotid bruits on auscultation. Then patient is lying supine, carotid sinus (located at level of thyroid cartilage) is gently palpated in a circular motion

Question 24

What is meant by synchronised cardioversion?

While on the topic, how is it performed?

Answer 24

Synchronised means that the defibrillator follows the patients rhythm to elicit a shock during the R wave of the QRS

Patient is supine (fasting if not emergency). 2 adhesive pads placed over
L - Over apex of heart
R - Upper chest below the clavicle
Defibrillator then synchronised to deliver shock during the R wave or QRS at the energy selected (typically 100-200J and increased as needed)

Question 25

What must you warn a patient about before giving them adenosine?

What is a life-threatening complication of adenosine? What patient cohorts are most susceptible to this?

Answer 25

Adenosine causes a deeply uncomfortable feeling for patients where they feel like they are going to die => warn them

May precipitate Ventricular fibrillation especially in patients with pre-existing Coronary artery disease or CABG

Question 26

You have just finished treating a patient with an SVT. The patient asks you what can they do to prevent another scenario like this again. What will you tell them?

Answer 26

1) Avoid triggers such as alcohol nicotine cocaine
2) Stress and anxiety management (education, counselling, mental health support)
3) Medication adherence to existing heart condition (if present)

Question 27

What are your differentials for an SVT or arrhythmia in general rly.

Basically: What are your differentials for this ECG

Answer 27

Obviously separate ventricular from atrial arrhythmias and tachy from brady.
So for atrial arrhythmias and tachycardia:
Sinus tachycardia
AVNRT
AVRT
Atrial tachycardia
MAT - Multifocal atrial tachycardia
SANRT - Sinoatrial nodal reentrant tachycardia
Atrial Fibrillation
Atrial flutter (atypical)

Question 28

A patient presents to the OPD with recurrent episodes of severe palpitations and dizziness but are self-limiting. She wants them to stop. Class II and Class IV antiarrhythmetics did not work, neither did the Class 1c drugs. You opt for surgical management with catheter ablation
What are you ablating?

What is the main complication of this procedure?

(if you dont know them go to the NC on medications in cardiology)

Answer 28

So this is a case of chronic SVT

Catheter ablation of the slow pathway hence only leaving fast and common pathways

AV block secondary to catheter ablation

Question 29

A patient presents to the OPD with recurrent episodes of severe palpitations and dizziness but are self-limiting. She wants them to stop. Class II and Class IV antiarrhythmetics did not work, neither did the Class 1c drugs. You opt for surgical management with catheter ablation of the slow pathway. unfortunately this ended with the complication of AV block secondary to catheter ablation. What does the patient need now?

Answer 29

Permanent pacemaker

Question 30

A patient presents to the OPD with recurrent episodes of severe palpitations and dizziness but are self-limiting. She wants them to stop. What will you prescribe them?

What if these medications fail? (Surgical)

Answer 30

So this is a case of chronic SVT => Pill in pocket approach
1) Class II Beta blocker Metoprolol OR Class IV CCB Verapamil Diltiazem
2) Class 1c Flecainide or Propafenone

Surgical: Catheter ablation of the slow pathway!!

Question 31

What is the main complication of an SVT?

Other complications in the realm of SVT (just putting them all in one place)

Answer 31

Main: Ventricular fibrillation with sudden cardiac death (whole thing)

AV block secondary to catheter ablation of the slow pathway resulting in permanent pacing

Least important: Toursades de points in Long QT syndrome which is a RF