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Cardio Block > Supraventricular Arrhythmias > Flashcards

Supraventricular Arrhythmias Flashcards

1
Q

What is the normal sinus rate range?

What can the sinus rate approach when under stress and exertion?

A

60-100 bpm

200bpm

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2
Q

How do you calculate a persons maximal heart rate during full exertion?

A

220-age

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3
Q

What is ectopy? What are the two general outcomes?

A

It is when other cells of the heart (outside of the sinus node) fire and capture the myocardium causing cardiac contraction.

  1. short burst of abnormal HR
  2. sustained arrhythmia
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4
Q

Beats that come before the next sinus beat are ______ whereas beats that arise from ectopic foci and occur after a pause in normal heart rhythm are called ______/

A

Premature beats; escape beats

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5
Q

What are the 3 locations that a premature or escape beat can arise from?

A
  1. atrial muscle cell (PAC, APB)
  2. specialized conducting tissue (AV, His, Purkinje)
  3. ventricular muscle cell (PVC, VPB)
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6
Q

What are the two main causes of arrhythmia?

A
  1. abnormal automaticity- beats from single focus that have increased phase 4 depolarization
  2. Triggered beats- beats from a single focus that occur early in depolarization (3 or 4) and cause more APs
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7
Q

Abnormal automaticity is due to changes in what?
They can lead to what?
Are they from a single focus or multiple foci?

A

they are due to changes in phase 4 depolarization
They lead to SVT from ectopic sites.
They are from a single focus and can cause spontaneous arrhythmia or drug toxicity

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8
Q

What are triggered beats? How are they similar and different to automaticity?

A

Like automatic rhythms, they arise from a single focus and can cause certain spontaneous and drug-toxic arrhythmias.
They differ in that they are triggered by the depolarization of the beat before (* they do not have pacemaker function like automaticity)

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9
Q

What are the two types of triggered beats? How do they differ?

A
  1. EAD- early after depolarization beat is related to a prolonged AP lengthening the plateau. they can be single or multiple AP
  2. DAD-delayed after depolarization occurs after repolarization of the AP and results in another rapid depolarization (can be subthreshold or suprathreshold)
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10
Q

What is the most common mechanism for cardiac arrhythmia?

A

Reentry- when an electrical impulse travels from one location to another and then returns to the start point via another pathway. If conduction persists, it causes tachycardia.

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11
Q

What are the requirements for reentry to occur?

A
  1. Two pathways (functionally or anatomically distinct.. can be close to or far from each other)
  2. unidirectional block in one pathway (due to refractoriness)
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12
Q

Describe the process of reentry.

A

Normally, a single beat conducts down two pathways and when the two impulses collide, they extinguish each other.
If there is a premature beat (automatic or triggered), the impulse may find one pathway to be refractory and be blocked.
It will travel down the non-refractory pathway and then by the time it does, the second pathway will be excitable again. The impulse can then reenter via the second pathway.

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13
Q

Once reentry has been initiated, how long will it persist?

A

Until it reaches an impulse block at which point it will paroxsymally terminate.

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14
Q

What is the conduction rate and refractory period for A and B pathways?

A

A- slow conduction, fast refractory

B- fast conduction, long refractory

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15
Q

The symptoms of SVT are quite variable from asymptomatic to mild malaise to syncope. Most often, though, SVT presents with one or more of what 5 symptoms?
Which is the MOST common symptom associated with arrhythmias?

What do you have to do to define whether these symptoms are attributed to an arrhythmia?

A
  1. Lightheadedness
  2. Palpitations- most common symptom (awareness of ones beating heart –fluttering, pounding, thumping, skipping beats)
  3. Dyspnea
  4. weakness
  5. chest pain

Get an EKG during symptoms

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16
Q

What do the degree of symptoms often correlate to for SVT?

A
  1. HR- faster = worse they feel

2. Underlying cardiac abnormality

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17
Q

What is decreased BP in supraventricular tachycardia usually due to?
What two symptoms does this account for?

A

The increased rate of heart beats decreases the LV filling time so there is less CO and thus, low BP (weakness and lightheadedness)

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18
Q

When HR increases it is due to ___________ because _________ is fixed.

A

less diastole (filling time) because systole is fixed.

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19
Q

What is the pounding sensation (palpations) due to?

A

Cannon a waves- contraction of the atria and ventricle simultaneously (contraction against a closed tricuspid valve)

20
Q

Desribe the pulse for:

  1. supraventricular arrhythmias
  2. atrial flutter
  3. atrial fibrillation
A
  1. regular for most
  2. regular or irregular depending on conduction to ventricles
  3. irregularly irregular meaning that the heart rhythm is irregular and there is no pattern
21
Q

With SVT, A flutter and A fib, why is a radial pulse difficult to take?

A

There is variable diastolic filling time, so there end diastolic pressure is variable making pulse pressure (systolic-diastolic) variable

22
Q

With arrhythmias, the elevated rate alone is responsible for _________.Hemodynamic compromise like decreased BP and CO can account for________ and __________.

A

rate- palpitations

decreased BP and CO - lightheadedness/malaise

23
Q

What is a cannon A wave?

What is it strongly suggestive of?

A

Neck pounding due to the simultaneous timing of A and V contractions during AV nodal reentrant tachycardia

24
Q

What are the three major types of SVTs?

What are the 2 types of atrial arrhythmias?

A
  1. AV nodal reentrant tachycardia
  2. AV reentrant tachycardia (WPW)
  3. Atrial tachycardia
  4. Atrial flutter
  5. atrial fibrillation
25
Q

What are the EKG characteristics of WPW (AV reentrant tachycardia)?

A
  1. Delta waves
  2. short PR (less than 0.12)
  3. prolonged QRS
26
Q

What is the cause of the delta wave on the WPW EKG?

A

There is an accessory pathway (AP) that connects the atrium and the ventricle (not through AV node).
It short circuits the AV conduction because it has more rapid conduction properties (similar to myocardium).
This slurs the upstroke of QRS because the PR interval is essentially eliminated

27
Q

What is the mechanism by which WPW syndrome occurs?

What will the EKG look like?

A

In normal sinus beat pattern, conduction goes down AV and AP connections (they extinguish each other)
In premature beat (automatic or triggered) the impulse may block in the AP and continue in the AV node. This would yield a normal P wave, PR interval, and narrow QRS.
If the AV node is blocked and the AP is used, there will be a shorter PR interval and a slightly widened QRS

28
Q

What are the two types of AV reentrant tachycardia pathways in WPW?

A
  1. Orthodromic where the ventricles are activated down the normal conduction system (down AV, up AP)
  2. Antidromic- the ventricles are activated via the AP and the reentry occurs in the AV node
29
Q

The delta wave is created by pre-excitation of the ventricle tissue adjacent to the ___________.

A

Accessory pathway (hatched area).

30
Q

What is AVNRT?
How is it similar to AVRT (like WPW)?
How is it different?

A

AV node reentrant tachycardia. It is like AVRT because it is a narrow QRS complex tachycardia exceeding 150bpm.
It differs, however, in that the sinus rhythm is normal because both limbs of the reentry pathway are in the AV node, and connect to His-Purkinje

31
Q

Describe the mechanism of AVNRT.

A

There are 2 pathways in the AV node. “slow” and “fast”.
With a normal sinus rate beat, the impulse goes down both pathways.
If there is a premature beat, the fast pathway blocks (because it is still refractory) and the slow conduction still occurs. This prolongs the PR interval.

32
Q

With AVNRT, describe the EKG when the heart is in normal sinus rhythm.

What happens on the EKG with a PAC?

What happens if an AVNRT starts?

A

The EKG will be normal with a slightly shorter PR interval because even though there are 2 pathways throught the AV node, only the ‘fast’ will be visible.

If there is a PAC, the fast pathway will be blocked and the conduction will travel through the slow pathway. The PR interval will be long.

If a AVNRT starts, there will be no clear P waves anymore due to the lack of involvement of the atrium

33
Q

What is treatment for AVNRT?

A
  1. Stop or slow the arrhythmia with electrical or chemical cardioversion
  2. Block AV conduction with B blockers, Ca channel blockers, digoxin
  3. Repeat EKG
34
Q

What are the causes of atrial tachycardia?
What is the frequency of this event (as compared to AVRT or AVNRT?
What is the heart rate range for atrial tachycardia?
What is the ratio between atrial conductions and ventricular conductions?

A

It is less common than AVRT or AVNRT. It is caused by:

  1. Automaticity
  2. Reentry
  3. triggered activity at a distinct atrial focus

The HR is between 150-250 and there is a 1:1 conduction to the ventricles

35
Q

For paroxysmal supraventricular tachycardia (PVST) what would you expect if:

  1. there was no P wave
  2. you saw delta waves
  3. P wave AFTER QRS
  4. HR of 150 BPM
A
  1. AVNRT- because atrium and ventricles would depolarize at the same time
  2. AVRT (WPW)
  3. AVRT
  4. look for atrial flutter suggestive of a 2:1 a to v conduction
36
Q

What is atrial fibrillation believed to be the result of ?

What specific area of the atrium has become a target for ablation?

A

multiple, ever-changing reentrant wavelengths involving both atria. Specifically around the pulmonary veins (a target for ablation)

37
Q

Describe the EKG of atrial fibrillation.

A

There are no distinct P waves (because of multiple foci beating at 350-500bpm) and there are irregularly irregular ventricular response (with narrow QRS) at about 100-170 BPM

38
Q

What are the 3 time frames for atrial fibrillation?

A
  1. Paroxysmal - self-initiating and terminating and lasts less than a week
  2. Persistent- lasts more than a week and requires intervention to terminate
  3. Chronic/permanent- accepted as the final rhythm
39
Q

Atrial fibrillation in the setting of _________ creates a potentially life threatening circumstance.

A

WPW because instead of the AV node only conducting certain pulses to the ventricle, the accessory pathway conducts rapidly to the ventricle resulting in a rapid beat that can cause low BP, syncope and death

40
Q

What is it called if atrial fibrillation is seen is a structurally normal heart?

A

lone atrial fibrillation

41
Q

Atria that are fluttering or fibrillating have _____________ atrial contraction which leads to a risk of _______________..

A

Weak or ineffective atrial contraction which leads to a risk of thrombus formation and possible ischemic stroke due to embolization

42
Q

What are the CHADS2 Risk Criteria?

A 
CHF-1
Hypertension- 1
 (age) Over 75 -1
DM- 1
Stroke or embolic event in the past -2

0- aspirin (80-325mg)
1- aspirin or warfarin
2 and up- warfarin (INR 2 to 3)

43
Q

What are the 3 main goals of treatment for atrial fibrillation?

A
  1. rate control (keep ventricle below 100bpm)
  2. rhythm control
  3. prevent thromboembolism

Controlling HR and controlling rhythm have the same mortality

44
Q

In typical atrial flutter, what is the cause of the tachycardia?
What is the atrial rate? what is the conduction to the ventricle?
What is the characteristic EKG pattern?

A

reentry encircling the tricuspid annulus (up the septum and down the right atrium wall) at a rate of 250-350 bom
There is a 2:1 conduction to ventricles so the ventricle rate is about 150bpm

The EKG shows a sawtooth pattern

45
Q

What are the typical causes of atrial flutter?

A 
Hypertension
cardiomyopathy
ethanol
Ischemic heart disease
valvular heart disease
metabolic problems
46
Q

How is definitive diagnosis of an arrhythmia made?

A

Invasive electrophysiology study (EPS)

  1. Electrodes placed in central veins, atrium, ventricle, coronary sinus, His bundle region
  2. Pacing and recording allows a map of abnormal circuits

Cardio Block (25 decks)

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