SVT - Supraventricular Tachycardia Flashcards
What is the normal electrical activity of the heart?
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)
Where does the SA node lie?
Right atrium
Define SVT
What is the pathophysiology of SVT
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.
List the 5 types of SVT
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
SVT may be persistent or paroxysmal (intermittent). How does a broad complex SVT occur?
If there is SVT + Bundle branch block -> Broad complex tachycardia
If just SVT, it is narrow complex
List the 3 main types of SVT along with a brief definition/description of what each is.
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
The AV node has 2 pathways. What are these pathways?
Then explain them in the context of AV nodal re-entrant tachycardia
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
What is meant by the term sinus tachycardia
Means everything is normal including the presence of all components except the fact that the rate is >100bpm
How would an ECG of typical SVT look like?
Regular Tachycardia + Absent P waves (embedded or inverted in inferior leads), Narrow QRS <80
what is the normal PR, QRS, and QT intervals
PR - 120-200ms/0.12-0.2s
QRS - 80-100/120ms
QT - 350-450ms
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?
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
What is significant about the epidemiology of SVT?
F>M
It is a common tachycardia in young females
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.
Palpitations
Syncope/pre-syncope
SOB/Dyspnoea
Chest pain
Fatigue
! feeling of rapid neck pulsation !
How does an arrhythmia cause SOB/dyspnoea and chest pain?
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
What is Long QT syndrome
What can it lead to?
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
What medications may cause long QT syndrome?
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)
Briefly, what is Torsades de Points?
It is a type of ventricular tachycardia whereby QRS complexes appear to rotate around the baseline
List the RFs for SVTs
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)
What are the signs of SVT?
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
What investigations will you carry out for an SVT
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)
How would you manage an acute narrow complex tachycardia (SVT)
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
How is the valsalva manouvre performed?
Patient blows into a syringe to blow plunger away
Briefly explain what a carotid sinus massage is and how it is performed
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
What is meant by synchronised cardioversion?
While on the topic, how is it performed?
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)
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?
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
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?
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)
What are your differentials for an SVT or arrhythmia in general rly.
Basically: What are your differentials for this ECG
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)
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)
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
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?
Permanent pacemaker
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)
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!!
What is the main complication of an SVT?
Other complications in the realm of SVT (just putting them all in one place)
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
