Ventricular Arrhythmias Flashcards by Aboudi el masri

What are the 3 main types of ventricular arrhythmias?

NSVT - Non-sustained ventricular tachycardia
VT - (sustained) ventricular tachycardia
VF - Ventricular fibrillation

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Define a Non-sustained VT

Define VT

What are the characteristic features on ECG

NSVT - 3+ consecutive broad complexes with a HR>100/120, and lasting <30s.

VT - 3+ consecutive complexes, HR>100/120, lasting >30s

Broad QRS complexes (>120ms) with AV dissociation (P and QRS are dissociated)

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What are the reversible causes of ventricular arrhythmias?

6Hs and 6Ts
Hs: Hypothermia, hypoxia, hypovolemia, hypoglycemia, hypomagnesia, hyper/hypokalameia

Ts: Thrombosis (MI,PE), Trauma, Tamponade, Tension pneumothorax, long qT medications (Class Ia, III, macrolides, methadone, antidepressants and antipsychotics), Toxins

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What are the main RFs/causes of Ventricular Arrhythmias (all similar)

Include the reversible causes

Cardiac:
Aortic dissection
Myocarditis
Ischaemia (MI) - Thrombosis
Cardiac Tamponade

Resp: PE (Thrombosis), (Tension) pneumothorax

Neuro: Stroke, Seizure

Electrolyte: Hypomagnesia, Hypo/Hyperkalaemia, Hypoglycaemia (i know its not an electrolyte)

Environmental: Trauma, Hypothermia, Hypoxia (drowning), Electric shock

Drugs: Long QT drugs (Class Ia, III, macrolides, methadone, antidepressants and antipsychotics)

Other Hs: Hypovolaemia, hypoglycaemia

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What is the pathophysiology of NSVT?

In healthy individuals - Reactivation of Na and Ca channels

In patients with significant previous cardiac disease - Damaged myocardium leads to cardiac remodelling leading to re-entrant impulses causing arrhythmia (just like in A.fib)

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What is the pathophysiology of VT

VT arises from an impulse either from the ventricular myocardium and/or anywhere distal to the bundle of his (as opposed to SVT), resulting in re-entry pathways

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Long QT syndrome will cause what morphology of Ventricular tachycardia?

Long QT syndrome causes Toursades de Points which is a Polymorphic VT
It literally changes from positive deflection to -ve deflection => polymorphic

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Ventricular tachycardia is unpredictable and a life threatening event => it is important to make distinctions in:
Duration:
Morphology:
Associated symptoms:
Associated Cardiac disease:
For each of the above, make these distinctions explaining how.

Duration: Sustained (>30s) vs Not sustained (<30s)
Morphology: Monomorphic vs Polymorphic (post-MI or Toursades de Points) - are all the QRS the same shape?
Associated symptoms: None, Haemodynamic instability, collapse.
Associated Cardiac disease: Non-malignant vs Malignant (CHD, MI, cardiomyopathy)

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What is the significance if making the distinction if a VT is malignant or not?

Malignant (=associated cardiac disease such as CHD, MI, cardiomyopathy) increases the risk of cardiac arrest and sudden cardiac death

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Ddx for any arrhythmia (asymptomatic)

All the other arrhythmias of the same type b/w tachy and brady

=> SVT: A.fib, Flutter, AVNRT, AVRT, Atrial tachycardia, MAT (Multifocal AT), SANRT (SA nodal re-entrant tachy)
VT: NSVT, VT, VF

+ Electrical artifacts

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What are some examples of electrical artifacts

Tremor from parkinsons, MS, SABAs, hyperthyroidism, hepatic encephalopathy

patient movement
electrode movement

Dont take this question too seriously

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What are signs and symptoms of ventricular arrhythmias

Symptoms: Palpitations, syncope/pre-syncope, dyspnoea, chest pain

Signs:
Vitals: Rapid Irregular pulse/absent pulse, BP normal/low/absent
GI: Diaphoretic, LOC
CI: !! Cannon A waves
Auscultation:Variability in rhythm and intensity of heart sounds

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What is the typical presentation of Ventricular fibrillation?

Collapse with no CO => no pulse, no BP

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When are Ventricular fibrillations most likely to occur?

48-72 hours after the onset of symptoms presumably due to ischaemia or lack of perfusion to the infarcted vessel (e.g. post-MI)

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What are Cannon A waves?

Irregular JVP pulsations due to contraction of the right atrium against a closed tricuspid valve

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What investigations will you perform for ventricular arrhythmias

As for any arrhythmia: except ECG
Bedside:
ECG/!Holter monitor: looking for patterns consistent with NSVT, VT, or VF (specific questions will come) + screen for previous MI, BBB, or LV hypertrophy
Urine dipstick (sepsis)
Urinalysis (evidence of CKD to guide management between DOAC and Warfarin) + Toxicology (sympathetomimetics)

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)

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What is the typical length of QRS?
How about in VT?
What are the 3 types of QRS complexes seen on a VT ECG along with their relative QRS?

Normal QRS is 80-100 (or 60-120)
In VT it is widened => >120 in general

3 beats:
Normal VT beats&raquo_space;120
Fusion beat >120
Capture beat 80-120 or whatever variation of normal you choose

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What would an ECG of Ventricular tachycardia show?
Go through all the features

NSVT and VT are the same cuz the only difference is how long they last
Definition: 3 consecutive complexes, HR>100/120, for < or > 30s

Features:
1) Tachycardia >100/120
2) AV dissociation
3) Wide QRS >120 (in general)
4) 3 beats: VT, Fusion, Capture beat

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What is a fusion beat?

It is a hybrid beat caused by the atrial impulse coinciding with the ventricular impulse => QRS>120

as opposed to “normal” VT where it is just a ventricular impulse => widened QRS&raquo_space;120

What is a Capture Beat?

Atrial impulse breaking through despite ongoing VT => Normal QRS (80-100 or whatever normal wants to be)

as opposed to “normal” VT where it is just a ventricular impulse => widened QRS&raquo_space;120

What are the red arrows pointing at?

Locate the following in this image:
Normal VT beat
Fusion beat
Capture beat

Red arrows are pointing at P waves

What is the cardiac output in V.fib?
What are you expecting to find when taking their pulse?
What about their BP

0, all non-existent

How would you differentiate between VT and SVT by looking at an ECG? (just the name)

Brugada technique

What is meant by AV dissociation on an ECG?

No relation between P (atrial) and QRS (ventricle)

What is meant by the precordial leads?

They are leads V1-V6 which represent the anterior, septal, and lateral aspects of the heart

Using the Brugada technique, explain how you will tell if an ECG is representative of a VT rather than SVT?

The following indicate VT over SVT
1) Absence of RS complex in V1-V6
2) RS interval >100ms in V1-V6 (if it was present)
3) AV dissociation (no relationship between between P and QRS)
4) Morphology of VT in V1,V2, and V6: V1, V2 = notched QRS, V6 = normal morphology and wide QRS

You are an intern on the ward. The consultant asks you to describe brugada technique to differentiate SVT from VT. Obviously, you have no idea what that is or how to interpret the ECG. The consultant asks you, what can you perform to distinguish SVT from VT. What is the answer?

Electrophysiology Studies

One big box on an ECG is how many ms? How about small boxes?

Small box = 40ms or 0.
Large box = 200ms

How will you determine the HR on an ECG?

If rhythm is regular, 300/number of big boxes between R waves
If rhythm is irregular: it is the number of R waves on the rhythm strip x 10

why? a strip is 6s => 10x the strip in a minute

An inpatient at the hospital with a holter monitor shows 6 consecutive ventricular complexes at a HR of 150 bpm lasting 15 seconds. ECG shows wide QRS complexes and AV dissociation. You take a history of the patient and the patient was not aware of the incident. What is the most likely diagnosis?

How will you manage this patient?

Asymptomatic NSVT

Treat reversible causes (e.g. Mg, K+)

A patient presents with Pre-syncope and palpitations. ECG shows NSVT. What is the management of this condition?

Symptomatic NSVT
First thing is to check if the patient has any underlying cardiac disease.

If not: Reverse underlying cause -> Beta blocker or CCB -> Catheter ablation or Amiodarone if ablation not suitable

If yes: Reverse underlying cause + optimise existing therapy -> ICD

What is an ICD? How is it performed?

It is an implantable cardioverter defibrillator. It terminates a VT by overdrive pacing and/or cardioversion defibrillation

Local anasthesia, small incision. one or more leads are inserted via the subclavian or cephalic vein to the ventricle/atria. This is guided via fluoroscopy (X-ray guidance). The ICD generator/device is then placed in a small pocket under the skin and tested.

A patient presents to the ED with Pre-syncope and palpitations. ECG shows sustained VT. What is your approach to managing this patient? (Just the approach)

It is based on the presence/absence of a pulse and the stability of the patient

Pulseless: ABC + CPR-> IV adrenaline -> Defibrillator shock ->IV/IO amiodarone -> Defibrillation shock, repeated until ROSC -> Identify and treat reversible causes

An inpatient on the ward suddenly has severe palpitations and is having severe chest pain. The holter ECG is showing what is consistent with ventricular tachycardia. You check the pulse which is present and the patient is stable. The first line is giving IV procainamide or Lidocaine. How will you decide which to choose?

Procainamide is a type Ia anti-arrhythmic. It is preferred over lidocaine in most cases. However as a type Ia, it does prolong the QT interval => in cases where there is 1) prolonged QT,
2) toursades de points,
3) or HF
Lidocaine is chosen insted. It is a Ib anti-arrhythmic medication => shortens QT

What type of drug is amiodarone

What is the regimen you are using to administer this !in this case!?

What drug us given after that? Indicate its type and how it is administered.

IV amiodarone (Class III/K+ blocker) 150 mg in 10 minutes followed by 1mg/min for 6 hours followed by 0.5mg/min for 18 hours

different ways in different cases

IV sotalol (Class III/K+ channel blocker) 1.5mg/kg over 5 mins

When should Sotalol be avoided when treating a VT?

If long QT

Severe chest pain => analgesia (morphine/strong opioid)

Stable:
1) IV Procainamide/Lidocaine
2) IV amiodarone 150 mg in 10 minutes followed by 1mg/min for 6 hours followed by 0.5mg/min for 18 hours
3) IV sotalol 1.5mg/kg over 5 mins
4) Heparin + analgesia +/- sedation for Cardioversion

What is the difference between cardioversion and defibrillation shock?

Cardioversion is a synchronised shock administered during the QRS complex. In pulseless VT and VF, an unsynchronised defibrillation shock is administered

No CPR is done for pulseless patients
Rate would be 30:2 with bag mask

Pulse Present but Unstable:
1) ABCDE (no CPR)
2) -> Identify and treat reversible causes
3) -> Heparin + Amiodarone adjunct + Analgesia +/- Sedation for Cardioversion which is repeated until ROSC

What is the most likely diagnosis?

You are about to administer IV adrenaline. what regimen are you using in this case?

Pulseless VT or V.fib (yes so 2)

IV adrenaline 1mg every 3-5 minutes or every cycle

An inpatient on the ward suddenly has severe palpitations and is having severe chest pain. The patient then goes unconscious. The holter ECG is showing what is consistent with ventricular tachycardia. You check the pulse which is not present. You begin chest compressions and perform ABC. Adrenaline has been injected multiple times with no help. The next step is a defibrillator shock. If the device is monophasic, what is the power used? What about biphasic?

If the shock is administered and fails what should you do?

If biphasic -> 120-200J, Monophasic -> 360 J

If the first shock is not successful another shock is performed

An inpatient on the ward suddenly has severe palpitations and is having severe chest pain. The patient then goes unconscious. The holter ECG is showing what is consistent with ventricular tachycardia. You check the pulse which is not present. You begin chest compressions and perform ABC. Adrenaline has been injected multiple times with no help. 2 shocks are then administered with no resolve. The next step is IV/IO amiodarone or lidocaine. What is the regimen used in each case?

IV/IO amiodarone 1st dose 300mg, 2nd dose 150 mg or Lidocaine 1st dose 1.5mg/kg 2nd 0.75mg/kg

!!Emergency management as per ACLS guidelines with CPR and unsynchronised cardioversion!!
1) ABC + CPR
Begin chest compressions
A - Head tilt, chin life, Jaw thrust, suction +/- intubate
B - Bag mask valve 30:2 with minimal interuption
C - Obtain IV access -> IO

2) IV adrenaline: 1mg every 3-5 minutes or every cycle
3) Defibrillator shock repeated 2x: If biphasic -> 120-200J, Monophasic -> 360 J
4) IV/IO amiodarone 1st dose 300mg, 2nd dose 150 mg or Lidocaine 1st dose 1.5mg/kg 2nd 0.75mg/kg
5) Identify and treat any reversible causes (Hs and Ts) until ROSC

Describe the ECG for VF.

How does a VT progress into Vfib on an ECG

Rapid (300-400bpm) irregular, shapeless QRST undulations of variable amplitude and morphology.

Initially is VT then coarse waveforms
-> Reducing in amplitude to form Fine wave forms
-> eventually leading to Asystole

A patient with known chronic VT re-attends the ED after being discharged. What is the management for Chronic VT?

ICD +/- Amiodarone 200mg OD

What is the management of idiopathic VT?

Beta blocker/CCB -> Catheter ablation -> Amiodarone

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Ventricular Arrhythmias Flashcards

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