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CardioPulmonary Vascular Disease > Arrhythmia Electrophysiology > Flashcards

Arrhythmia Electrophysiology Flashcards

1
Q

The p-wave on EKGs represents what?

A

atrial depolarization

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2
Q

what is occuring during the PR interval?

A

AP through atria & AV node

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3
Q

what does the QRS complex represent?

A

ventricular depolarization

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4
Q

what is happening during the t-wave?

A

ventricular repolarization

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5
Q

The QT interval represents what?

A

duration of repolarization phase

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6
Q

Describe the 5 phases of ventricular AP?

A

0: Na channels open & major ion influx being sodium; 1: Na channels close; 2: Ca channels open slowly hence the plateau effect & major ion influx is calcium; 3: K channels open as Ca channels close; 4: K remain major ion influx as Na/K and Na/Ca antiport pumps attempt to reestablish the resting membrane potential

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7
Q

Compare & contrast the differences b/t supraventricular & ventricular arrhythmias.

A

SVT: originates at or above the His bundle; normal or narrow QRS & normal ventricular contraction; VT: originates below the His bundle; abnormal ventricular activation w/ wide QRS

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8
Q

what are the 2 categories for arrhythmia mechanisms?

A

Abnormal Impulse Initiation; Abnormal Impulse conduction

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9
Q

What are the 2 subtypes of abnormal impulse initiation?

A

abnormal automaticity; Triggered Activity

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10
Q

What are the 2 subtypes of abnormal impulse conduction?

A

conduction block; reentry

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11
Q

What are examples of altered normal automaticity?

A

Sinus tachycardia; sinus bradycardia; inappropriate sinus tachycardia

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12
Q

What are common causes of abnormal automaticity?

A

hypoxia, ischemia, inflammation: all of these conditions will increase the membrane potential and inactivate Na+ channels; inactivation of Na channels can transform cells that are normally fast response to slow response mediated by L-type Ca channels; this increases the cells’ ability to initiate their own action potentials independently of the SA node

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13
Q

Triggered activity arrhythmias are typically caused by what homoeostatic disturbances?

A

electrolyte imbalances

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14
Q

In cases where a pathological AP is triggered by a previous normal AP, what are the 2 most common changes seen on the potential curve?

A

Early afterdepolarization (EAD); Delayed afterdepolarization (DAD)

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15
Q

What is the electro pathophysiology of EAD?

A

premature re-opening of L-type calcium channels leading to a prolonged AP duration

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16
Q

what is the electro pathophysiology of DAD?

A

Ca2+ overload due to increased Na/Ca exchanger current

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17
Q

What is the qualitative definition of Reentry?

A

when the same electric impulse re-excites the heart again

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18
Q

What is assoc. w/ EAD?

A

prolonged AP duration, prolonged QT intervals & bradycardia; hypokalemia

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19
Q

conduction blocks cause what type of arrhythmias?

A

bradyarrhythmias

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20
Q

what 3 things must happen for a reentry to occur?

A

There needs to be some kind of unidirectional block; conduction also needs to be slowed; And recovery of previously excited proximal tissue

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21
Q

Would decreasing the conduction wavelength increase or decrease the risk of reentry?

A

It would increase risk of a reentry

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22
Q

What are different types of macro-re-entry?

A

AVRT; atrial flutter; ventricular tachycardia

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23
Q

what are different types of micro-re-entry?

A

AVNRT; atrial fibrillation & tachycardia; ventricular fib & tachy

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24
Q

there is always going to be an inverse relationship b/t ERP & AP duration; how does this apply to the concept of normal electophysiology?

A

Slow response cells such as the SA & AV nodes will have a high ERP and shorter AP duration; this makes it easier to initiate an AP but at the expense of longer recovery time to give the fast response cells time to recover before firing the next AP

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25
Q

what is the difference b/t mirco & macro reentry?

A

Micro: only invovles AV node; Macro: involves AV node + 1 accessory pathway

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26
Q

What is the direction of an anterograde current?

A

Atria to Ventricles or Base to apex; retrograde would be the reverse of this

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27
Q

Describe the electro pathophysiology of Wolff-Parkinson-White-Syndrome (WPW)

A

WPW is an example of AVRT: this type of reentry is caused by a an additional accessory pathway in the atrium that can bypasses the conduction velocity through the AV node; in other words, SA propagation is being split b/t the AV node & the accessory pathway; The CV of the accessory pathway in this case surpasses the CV of the AV node; hence the accessory pathway will excite the ventricular myocytes before the AV node does; this creates a reentry circuit where the accessory propagation also initiates the AV node

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28
Q

Describe the electro pathophysiology of AVNRT?

A

no accessory pathway involved but rather the AV node itself is directly involved; This happens when the currents that split from the AV node do not have the same AP duration & ERP; the current w/ the shorter ERP will propagate to the ventricles first; when the current of the slow ERP finally catches up, the faster current will already be in its RP and the current terminates; both pathways will go through their ERP and be ready for another AP propagation coming from the AV node

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29
Q

What if in addition to an AVNRT, there is also a premature beat? How will this change the electro pathophysiology?

A

Let’s use an example; lets say we have a pre-mature AP propagation while the fast track is still recovering but the slow tract is ready to be fired again. In this scenario the impulse is going to travel down the slow tract; by the time the fast track recovers it catches up with the impulse going down the slow tract; rather than termination of the impulse happening, in this case the impulse from the slow tract activates the fast track and goes back up to the atrium where it will activate the slow tract;

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30
Q

Atrial flutters & fibrillations are always going to be associated w/ which type of arrhythmia?

A

reentry supraventricular tachyarrhythmias

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31
Q

Arrhythmias with Narrow the QRS complex are always going to be what type?

A

supraventricular: originates at or above the AV node

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32
Q

Fibrillations & flutters are always going to have what EKG finding in common?

A

irregular rhythm

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33
Q

What is the most common culprit of atrial flutters?

A

cavotricuspid isthmus

34
Q

what is the most common culprit of atrial fibrillations?

A

pulmonary veins

35
Q

What accessory pathway is assoc. w/ AVRT?

A

Bundle of Kent at AV junction b/t Left Atrium & ventricle

36
Q

How does WPW affect EKG?

A

shortens the PR-intervals & widens the QRS complex w/ delta waves

37
Q

Why is WPW categorized as a SVT & VT?

A

WPW typically starts out a a type of ventricular preexcitation syndrome and can progress to a supraventricular arrythmia

38
Q

compare/contrast the differences b/t monomorphic & polymorphic VT.

A

monomorphic is typically assoc. w/ structural heart diseases; polymorphic VT is more commonly assoc. w/ channelopathies and electrolyte disturbances

39
Q

How do brady & tachy arrhythmias affect SV & HR?

A

Brady: increased SV assoc. w/ decreased HR
Tachy: decreases SV assoc. w/ increased HR

40
Q

How is conduction affected in Sinus Tachycardia?

A

conduction is not affected; usually caused by body’s normal response to pain, exercise, stress, & dehydration; secondary causes: anemia, hyperthyroidism, PE

41
Q

what are clues on EKG indicative of PACs?

A

variable p-wave morphologies assoc. w/ irregular rhythms

42
Q

How is Focal Atrial Tachycardia clinically defined?

A

regular atrial rhythm w/ impulses that originate outside the SA node

43
Q

What is the most common culprit of FAT?

A

left atrium

44
Q

What are EKG findings for FAT?

A

Rate: 150-250 bpm; regular rhythm; narrow QRS w/ normal PR intervals

45
Q

What are EKG indications of AVNRT & AVRT?

A

retrograde p-waves

46
Q

Antidromic AVRT affects the QRS complex how?

A

Widens QRS intervals

47
Q

A………AVRT travels down the BOK and then back up to the AV node.

A

antidromic

48
Q

A……AVRT travels down the AV node & then back up through the BOK.

A

orthodromic

49
Q

WPW Syndrome w/o pre-excitation will widen or shorten the QRS complex?

A

if pre-excitation is absent, then the QRS complex will be narrowed and therefore a SVT

50
Q

What is the most common site for A fibs?

A

LA near site of the pulmonary veins

51
Q

What does the CHA2DS2-VAS risk stratification assess?

A

Risk of Stroke; the higher the score the higher the risk

52
Q

List out the Acronym CHADSVAS.

A

C: CHF/LV dys.
H: HTN
A: Age > 75
D: DM
S: stroke/TED
V: vascular disease
A: Age 65-74
S: sex

53
Q

What are common EKG findings for MAT?

A

Variable P-wave morphology; very difficult to discern from A fib

54
Q

A pre-mature ventricular contraction is always assoc. w/ what?

A

Widened QRS Complex

55
Q

What is meant by the term Monomorphic VT?

A

Single ventricular ectopic pacemaker

56
Q

What EKG findings are indicative of a MVT?

A

Very wide QRS complexes with no flatlines; more like a sinus curve w/ identical amplitudes

57
Q

What is the qualitative definition for V fib?

A

Chaotic electrical activity from ventricles independent of CO

58
Q

What do V fibs look like on an EKG?

A

Variable morphology of the QRS complexes; no flat line; just continuous curves w/ variable different amplitudes

59
Q

What does Torsades de Pointes look like on an EKG?

A

Same as V fib but with the amplitudes are much bigger

60
Q

How is a First Degree AV heart block clinically defined?

A

Delayed conduction w/ no interruption; assoc. w/ prolonged but equal PR intervals

61
Q

What is another name for a 2nd degree heart block?

A

Mobitz (Wenckebach)

62
Q

What are the EKG findings of a 2nd degree HB? Type 1

A

Progressive Increase of PR intervals preceeding each QRS complex followed by a p-wave & absence of the QRS complex

63
Q

What are the EKG findings of a Mobitz Type II 2nd degree HB?

A

Prolonged BUT CONSISTENT PR interval w/ intermittent absence of QRS complex b/t

64
Q

What is the qualitative definition of a 3rd degree HB?

A

Atria and ventricles beat independently of each other

65
Q

What are the EKG findings of a 3rd degree HB?

A

Equal RR & PP intervals that are not synchronized w/ the QRS complexs

66
Q

How is the ventricular septum normally depolarized?

A

From left to right

67
Q

How does a LBBB affect the direction of ventricular depolarization?

A

Reversed: from right to left

68
Q

What EKG findings can help you distinguish b/t a R & L BBB?

A

Assess Lead V1; If the QRS complex is bimodal (2 distinct peaks) or biphasic then it is a RBBB; If the QRS complex is inverted then it is a LBBB

69
Q

How does hyperkalemia affect the QT intervals?

A

The duration of the QT depends on 2 things: Ventricular depolarization & repolarization; So in the case of hyperkalemia, you are decreasing the magnitude of the threshold making it easier to fire an AP thus shortening the QT interval;

70
Q

How does hypokalemia affect the QT interval?

A

IC K concentration is already much higher concentration to the EC K concentration; thus lowering the EC K concentration even more will increases the magnitude of the threshold making it harder to initiate an AP; hence, a longer QT interval

71
Q

How does hypercalcemia affect the QT interval?

A

Ca does not really come into play until phases 2 of the fast response AP; on an EKG this phase corresponds to the ST interval; during this phase the voltage stays the same causing the curve to plateau; this is b/c the voltage-gated Ca channels gradually open; therefore, if EC Ca levels are high then these channels are going to open at a much faster rate hence shortening the QT interval due to shortened ST

72
Q

How does hypocalcemia affect the QT interval?

A

Ca channels will open at a much slower rate during phase 2; hence, a prolonged ST segment which will prolong the QT interval

73
Q

Describe the electro pathophysiology of hypothermia?

A

Hypothermia results in sinus bradycardia w/ widening of the QRS complexes and prolongation of the PR & QT intervals; osborne J waves will also be seen

74
Q

what is the electro pathophysiology of Long QT Syndrome

A

reduced outward potassium current and increased inward sodium current leading to reopening of the L-type Ca channels as the ventricle repolarizes

75
Q

LQT risk is increased w/ what electrolyte disturbances?

A

hypokalemia; hypomagnesaemia

76
Q

Short QT syndrome is assoc. w/ what electrolyte disturbances?

A

hyperkalemia

77
Q

What is the electro pathophysiology of brugada syndrome?

A

diminished inward sodium current

78
Q

brugada syndrome is more common for what race and sex?

A

asian males

79
Q

what is the electro pathophysiology of catecholaminergic polymorphic VT (CPVT)?

A

leaky cardiac ryanodine receptors leading to Ca overload & DAD

80
Q

what are the EKG findings of brugada syndrome?

A

ST elevation in V1-V3

81
Q

What is the most common cause of Atrial fibrillation?

A

HTN!!!!!!!!

CardioPulmonary Vascular Disease (7 decks)

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