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Cardiology > Clinical Aspects Of Cardiac Arrhythmias > Flashcards

Clinical Aspects Of Cardiac Arrhythmias Flashcards

1
Q

Rate of less than 60 bpm w/ each P wave followed by a QRS and each QRS preceded by a P wave

A

Sinus Bradycardia

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2
Q

Sudden cessation of sinus node activity as evidenced by loss of atrial depolarization

A

Sinus arrest

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3
Q

What do we call a sudden cessation of sinus node activity if it is for

  1. ) Less than 3 seconds
  2. ) More than 3 seconds
A

Sinus Arrest

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4
Q

Resting sinus bradycardia with periods of supraventricular tachycardia often followed by sinus pauses or sinus rest

A

Brady-Tach syndrome

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5
Q

Diagnosed by a rate less than 60 bpm, w/ sinus pause or sinus arrest

A

Sick sinus syndrome

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6
Q

We can treat sick sinus syndrome w/

A

Atropine (anti-cholinergic), Beta agonists, and temporary pacemaker

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7
Q

Impaired conduction between the atria and ventricles

A

AV block

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8
Q

What are the three types of AV block?

A
  1. ) First degree
  2. ) Second degree
  3. ) Third degree
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9
Q

Characterized by a PR interval of greater than 0.2 sec w/ 1:1 relationship between P waves and QRS

A

First degree AV block

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10
Q

A 1st degree AV block can be caused by an

A

Inferior MI

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11
Q

There is usually no treatment see for a

-Avoid drugs that will cause further impairment

A

First degree AV block

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12
Q

Intermittent failure of AV conduction w/ some P waves not followed by QRS complex but constant P to P intervals and prolongation of PR interval before block

A

Mobitz type I 2nd degree AV block (Wenckebach)

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13
Q

An inferior MI, Lyme myocarditis, an congenital AV block can all cause

A

Wenckebach Block

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14
Q

For a mobitz I (Wenckebach) block, we may need to treat w/

A

Atropine or isoproterenol

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15
Q

Intermittent failure of AV conduction w/ some p waves not followed by QRS complex, constant P to P intervals and NO prolongation of PR interval before block

-QRS is usually wide

A

Mobitz Type II second degree AV block

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16
Q

An intermittent conduction block distal to the AV node in the bundle of His

A

Mobitz Type II

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17
Q

Clinically presents w/ syncope (Stokes-Adams), dizziness, extensive anterior MI

A

Mobitz Type II second degree AV block

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18
Q

Complete failure of conduction between atria and ventricle w/ NO relationship between p waves and QRS

-Sinus rate is greater than ventricular rate

A

3rd Degree Heart Block

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19
Q

Treated w/ a permanent pacemaker unless their is reversible AV nodal injury

A

3rd degree heart block

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20
Q

Normal, narrow QRS complexes at rates of 40-60 bpm w/ no p wave preceding the QRS

-May have retrograde p waves

A

Junctional Escape Rhythm (JESC)

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21
Q

Diagnosed by wide QRS complexes at rates of 30-40 bpm w/ no p wave preceding the QRS

-May have retrograde p waves

A

Ventricular Escape Rhythms (VESC)

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22
Q

Increased automaticity of the SA node by way of either increased sympathetic tone or decreased parasympathetic tone

A

Sinus Tachycardia

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23
Q

Premature p wave, usually followed by normal narrow QRS but can also be followed by wide (aberrantly conducted) or by no QRS

A

Atrial premature complexes

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24
Q

Can be caused by increased sympathetic tone, stretch, and fibrosis

A

Atrial Premature Complexes

25
Q

Atrial Premature Complexes (APCs) are usually followed by normally conducted

A

Narrow QRS complexes

26
Q

When the APC are very premature and fail to conduct to the ventricles or conduct w/ an aberrantly conducted complex due to block in the right or left bundle

A

APC w/ aberrancy and blocked APC

27
Q

Rate greater than 100 bpm w/ p wave morphology that is different than typical sinus p wave morphology

-sudden onset and termination

A

Atrial Tachycardia

28
Q

Can be the result of abnormal automaticity, DAD, or reentry

A

Atrial Tachycardia

29
Q

Treated w/ beta blockers, Ca2+ blockers, class IC or III antiarrhythmic drugs, or ablation

A

Atrial Tachycardia

30
Q

Rapid, regular, uniform atrial activity at a rate of 240-300 bpm

-Inferior leads have “Saw-tooth” appearance

A

Atrial Flutter

31
Q

Caused by reentry along the tricuspid valve annulus

A

Atrial Flutter

32
Q

An atrial flutter will often present w/ a

A

2 to 1 Block

33
Q

Irregularly irregular rate w/ no discernible p waves on the ECG but w/ low amplitude oscillations

-Presenting ventricular rate is usually 140-160 bpm

A

Atrial Fibrillation

34
Q

Multiple wandering atrial reentrant circuits w/ atrial rate

-Pulmonary vein triggers may initiate

A

Atrial Fibrillation

35
Q

Associated w/ hypertension, cardiomyopathy, CHF, mitral stenosis, mitral regurgitation, and ischemic heart disease

A

Atrial Fibrillation

36
Q

Acutely, we want to treat atrial fibrillation w/

A

Beta-blockers and Calcium-blockers

37
Q

For chronic treatment of atrial fibrillation, we want to give meds for which 3 purposes?

A
  1. ) Anticoagulation
  2. ) Rhythm control
  3. ) Rate control
38
Q

The sudden onset and termination of heart rates between

A

140and 250 bpm

39
Q

Regular, rapid, usually narrow QRS complex rhythm at rated of 140-250 bpm

A

AV nodal reentrant tachycardia

40
Q

Acutely, we can treat AV nodal reentrant tachycardia w/

A

Vagal maneuvers and adenosine

41
Q

Characterized by a short PR interval (less than 0.12 sec) w/ normal sinus p waves, wide QRS, and a delta wave that slurs first portion of QRS

A

Ventricular Pre-excitation (Wolff-Parkinson-White Syndrome WPW)

42
Q

Rapid conduction across the bypass tract and down the AV node w/ varying degrees of fusion

A

Atrial fibrillation in WPW

43
Q

Premature QRS complex, which is wide, because the impulse travels from its ectopic site through the ventricles via slow cell-to-cell connections

A

Ventricular Premature Complexes

44
Q

W/ a ventricular Premature Complex, the ectopic complex is not related to a

A

Preceding P wave

45
Q

Defined as more than 3 consecutive PVC at greater than 100 bpm

A

Ventricular tachycardia

46
Q

Rapid, wide QRS complex rhythm at rats of 100 to 300 bpm w/ all QRS complexes having the same morphology

A

Sustained Ventricular Tachycardia

47
Q

Consecutive wide QRS complexes w/ continually changing shape and rate from complex to complex

A

Polymorphic Ventricular Tachycardia

48
Q

ECG shows irregular deflections of varying amplitude and contour w/ no defined P waves, QRS complexed, or T wavs can be recognized

A

Ventricular Fibrillation

49
Q

Characterized by multiple reentrant circuits and clinically presents as cardiac arrest

A

Ventricular Fibrillation

50
Q

The cause of congenital long QT syndrome is an

A

Ion Channel Mutation

51
Q

Characterized by a coved type ST elevation

A

Brugada syndrome

52
Q

Characterized by a saddle-back type ST elevation

A

Brugada Syndrome

53
Q

Characterized by a very mild saddle-back “ST elevation”

A

Type 3 Brugada Syndrome

54
Q

A genetic arrhythmogenic disorder characterized by a peculiar ECG pattern

A

Brugada Syndrome

55
Q

Predisposes to ventricular arrhythmias and sudden cardiac death

-Affects males much more than females

A

Brugada Syndrome

56
Q

Caused by a mutation in genes coding for Calcium handling by proteins

A

Familial catecholaminergic polymorphic ventricular tachycardia

57
Q

Long QT 1 is triggered by

A

Exercise (swimming)

58
Q

Long QT 2 is triggered by

A

Auditory stimuli

59
Q

Long QT 3 often occurs at

A

Rest

Cardiology (27 decks)

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