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Cardio Block > Ventricular Arrhythmias > Flashcards

Ventricular Arrhythmias Flashcards

1
Q

What are “isolated ectopic beats”?

IF the ectopic beats are not isolated, what is that called?

A

Isolated would be:

  1. PAC
  2. PVC
  3. premature Junctional complex

If it is not isolated, it is an ectopic rhythm where the ectopic focus fires constantly

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2
Q

What is the EKG morphology of a PVC?

A

They are ectopic beats in the ventricles so they have wide QRS morphology (spread myocyte to myocyte instead of using His-Purkinje)

They usually have a compensatory pause, and then sinus rhythm starts again

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3
Q

What is a PVC couplet?

How does it differ from bigeminy?

A

Couplet- 2 PVCs in a row

Bigenimy- alternating PVC and normal sinus beat

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4
Q

How do patients usually describe PVCs to you?

A

“extra beat”- awareness of the PVC

“skipping beat”’ awareness of the compensatory pause after the PVC

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5
Q

What are normal causes of PVC and what is the treatment?

A

Can occur in normal hearts or with all types of cardiac disease and do NOT usually require treatment

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6
Q

If a PVC occurs during ventricular repolarization, what can occur?

A

If the PVC falls on the T wave, it is likely to progress to a more serious ventricular arrhythmia ESPECIALLY in the context of MI, ischemia, or prolonged QT

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7
Q

If there are 2 premature ventricular complexes in a row it is called ________. If there are three it is called _________. If there is more than 3 it is called _______.

A

2- couplet
3- triplet
>3- NSVT (non-sustained ventricular tachycardia)

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8
Q

What is the rate of ventricular tachycardia?
What categorizes something as a ventricular tachycardia?
What does the EKG waveform look like?

A

110-250bpm
If there are three or more PVCs that is considered a ventricular tachycardia.
There is a wide QRS complex (over 0.12s) and they can be monomorphic (from one ectopic site) or polymorphic (from multiple ectopic sites)

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9
Q

VT can be associated with only ______ but sustained VT often leads to _____________ particularly in those with ______________.

A

palpitations
hemodynamic collapse
LV dysfunction

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10
Q

What are the potential mechanisms of VT?

A
  1. reentry
  2. automaticity
  3. triggered beats
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11
Q

VT can be identified on EKG by two manifestations of the ectopic beats arising from the ventricles. What are they?

A
  1. AV dissociation- separate atrium and ventricle rhythm
  2. Fusion beats- if a sinus beat captures some of the ventricular myocardium from the ectopic ventricular focus, there will be a change in morphology that looks like a hybrid of normal sinus beat and ectopic ventricular beat
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12
Q

What is the difference between a fusion beat and a capture beat? What are they seen in?

A

They are seen with ventricular tachycardia.
Fusion beat- if the normal sinus rhythm from the atrium captures some of the ventricular myocardium, there will be a fusion beat (half ectopic, half normal sinus QRS)
Capture beat- if the sinus beat conducts through and captures ALL the ventricular myocardium, there will be a normal sinus QRS on the EKG

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13
Q

What is ventricular fibrillation?

What is it ALWAYS associated with?

A

It is a chaotic rhythm

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14
Q

What is ventricular fibrillation?

What does it ALWAYS present with?

A

with low amplitude undulating electrical activity in the ventricle myocardium.
It is ALWAYS associated with circulatory collapse.

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15
Q

What are the 3 types of VT or VF associated with a normal heart?

A
  1. Idiopathic left VT
  2. Idiopathic VF
  3. Outflow tract VT

All are relatively uncommon

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16
Q

What are the 3 types of genetic arrhythmia syndromes associated with VT and VF?

A
  1. Brugada
  2. Hereditary Long QT Syndrome
  3. Hypertrophic and Arrhythmogenic RV cardiomyopathy
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17
Q

What are the 3 main environmental assocations with VT and VF?

A

.1. Hypokalemia

  1. Hyperkalemia
  2. Drug-induced LQTS
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18
Q

What are the 2 LV dysfunctions associated with VT and VF?

A
  1. Ischemic cardiomyopathy

2. Non-ischemic cardiomyopathy

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19
Q

What are the characteristics of an Outflow Tract VT? (what focus does it arise out of, what are the morphology of the beats)

A

It arises out of a single focus in the RV or LV outflow tract region of the myocardium and has the same morphology for each beat (repetitive, monomorphic beat)

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20
Q

What is the EKG appearance of RVOT ventricular tachycardia?

A

It will head toward the inferior leads (II, III, avF) and will depolarize the RV first so it will give the appearance of a LBBB.

21
Q

What is the EKG appearance of a LVOT ventricular tachycardia?

A

It will head toward the inferior leads (+II, III, avF)

It will depolarize LV first so it will give the appearance of RBBB

22
Q

Outflow Tract VT typically arises in the setting of a _____________ and is due to ____________..

Who is the “typical patient” for OT VT?

A

It arises in a normal heart due to triggered activity (by increased adrenergic tone)

It is the presence of sustained palpitations near syncope in a 25-35 year old patient just after exercise or during exercise.

23
Q

What are the 2 drugs and one technique that can be used to treat OT VT?

A
  1. adenosine
  2. b-blocker

radiofrequency catheter ablation

24
Q

What is the cause of Idiopathic LV tachycardia?

What is the EKG presentation?

A

It occurs in a normal heart due to a macro-reentrant circuit in the left ventricular septum that utilizes a component of the left fascicle.

The tachycardia has a right bundle, superior axis morphology.

25
Q

What is used to treat an idiopathic Left VT?

What is the drawback of using it?

A

Verapamil- a Ca channel blocker
Verapamil can cause hemodynamic collapse in other forms of VT so you have to be POSITIVE that it is an idiopathic Left VT

26
Q

What is the “typical patient” for idiopathic left VT?

A

They present similarly to OT tachycardia, but it does NOT occur in short burst and is NOT associated with exercise.

It occurs in slightly older patients and there is palpitations and near syncope

27
Q

Hereditary LQTS is an __________ disorder caused by mutations in genes encoding ______________ that control _____________.

A

autosomal dominant
prominent ion channel complexes
cardiac action potential

28
Q

There are a variety of mutations that can cause hereditary LQTS. What do all the mutations have in common?
What can this lead to?

A

They all prolong the repolarization phase (3) of the AP which increases likelihood for triggered activity and can lead to polymorphic VT (torsades de pointes)

29
Q

What is Torsades de Pointes?

A

Long QT can lead to polymorphic VT where every QRS is slightly different and it looks like twisting ribbon

30
Q

What are the 3 most common genetic defects causing LQTS?

A
  1. LQT1 (KCNQ1- K channel, voltage gated)
  2. LQT2 (KCNH2- K channel, voltage gated H2)
  3. LQT3 (SCN4B- Na channel)
31
Q

What is the EKG finding of LQT1?

What activity is it associated with?

A

There will be a broad T-wave.

It is associated with exercise (usually swimming)

32
Q

What is the EKG finding of LQT2?

What activity is it associated with?

A

There is a notching of the T wave and is associated with abrupt changes in level of arousal (like a ringing alarm clock)

33
Q

What is the EKG finding of LQT3?

What activity is it associated with?

A

It will have peaked T waves and usually occurs during rest or sleep.

34
Q

What are the main therapies for LQTS?

A
  1. B-blocker for carriers of the disease

2. ICD (implantable cardioverter defibrillator) for patients with recurrent syncope and cardiac arrest.

35
Q

What is Brugada syndrome?
What genetic disorder is it “opposite” to ?
What can it lead to?

People of what descent are most likely to have this?
When do “attacks” usually occur?

A

An autosomal dominant genetic disorder associated with premature repolarization (the opposite problem with LQTS).
It is usually an abnormality in cardiac Na channel.

This can lead to V. fibrillation because there is heterogenous repolarization across the ventricle.

SE Asians and the attacks are most often at night

36
Q

Describe the EKG findings associated with Brugada Syndrome?

A

ST-elevation and T wave inversion in V1 and V2 in the setting of RBBB

37
Q

What is the therapy for Brugada Syndrome?

A

ICD (implantable cardioverter defibrillator)

DO NOT USE B-BLOCKER

38
Q

Who is likely to develop hypo or hyperkalemia that leads to VT or VF?

A

Patients with severe renal disease or those on aggressive diuretics for CHF

39
Q

What drugs are most likely to cause drug-induced LQTS which leads to Torsades de Pointes?

A
  1. antiarrhythmia class Ia and III
  2. antipsychotics
  3. antidepressents
40
Q

In the setting of ischemic heart disease, VT or VF can occur in the presence OR absence of an acute ischemic episode.
How can VT or VF occur in the presence of an acute episode? Which is more common, VT or VF?

What is the mechanism by which VT or VF occurs in the absence of an acute ischemic event? What is more likely to occur, VT or VF?

A

Myocardial ischemia will alter channel function changing the cells refractoriness or automaticity. This can lead to VF (more commonly than VT)

If there is not acute ischemia, reentrant VT is more common due to reentry within scar of a prior MI

41
Q

What are the main causes of VT and VF from non-ischemic heart disease?

A
  1. altered refractoriness
  2. conduction due to intrinsic myocellular disease
  3. conduction changes due to ECM and fibrosis

Which all increase the likelihood of reentry, triggered activity and automaticity.

42
Q

Over 75% of sudden cardiac deaths are due to what?

What are the other 25% due to?

A

VT of VF mostly in victims with coronary artery disease

25% due to bradyarrythmia (asystole, AV block)

43
Q

What is the preferred preventative strategy for SCD?

A

ICD- implantable cardioverter defibrillator

44
Q

What is the single greatest risk factor for SCD?

A

EF < 0.4 is at an elevated risk.

EF <0.3 is the most robust marker

45
Q

What are the EKG findings that show a patient is at increased risk for sudden cardiac death?

A
  1. complex ventricular ectopy (PVCs)

2. nonsustained VT (3-30 consec. beats)

46
Q

What makes it difficult to identify large groups that can benefit from preemptive ICD in a cost-effective manner?

A

Patients at the highest risk (EF<0.4 in post MI setting) represent the small minority of total SCD victims.

47
Q

What is the difference between primary and secondary prevention for SCD?

A

Primary- the person has risk factors but has not yet had an acute SCD event.
Secondary- the person has already experienced SCD and we need to prevent another

48
Q

How does an ICD work?

A

It is implanted like a pacemaker and records heart rhythm. It can deliver therapy (anti-tachycardia pacing to terminate VT) and delivers an electrical shock to terminate VF.

Cardio Block (25 decks)

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