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Flashcards in Arrhythmias Deck (103)
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1
Q

Premature Atrial Complexes, the beat arises from…

A

within the atria

2
Q

What do premature atrial complexes look like on ECG?

A

Early P waves with different morphology than the normal sinus P wave; QRS is normal

3
Q

Premature Atrial Complexes are usually asymptomatic but when symptomatic may cause….

A

palpitations or give rise to PSVTs

4
Q

If premature atrial complexes are symptomatic, how can they be treated?

A

Beta Blockers

5
Q

Causes of premature atrial complexes:

A
Adrenergic excess
drugs
alcohol
tobacco
electrolyte imbalance
ischemia
infection
6
Q

Premature Ventricular complexes

A

Early beat from a focus in the ventricle that then spreads to the other ventricle. PVCs can occur in patients with or without structural heart disease

7
Q

Causes of premature ventricular complexes:

A
Hypoxia
electrolyte abnormalities
stimulants
caffeine
medications
structural heart disease
8
Q

Premature Ventricular complexes on ECG

A

Wide, bizarre QRS followed by a compensatory pause

***Wide QRS because conduction is slower because it is not going through the normal conduction pathways, but through ventricular muscle

9
Q

Most patients with premature ventricular complexes are asymptomatic, but if symptomatic experience:

A

palpitations

dizziness

10
Q

If PVCs are symptomatic, may treat with

A

Beta Blockers

11
Q

Patients with frequent PVCs and underlying heart disease are at increased risk of

A

Sudden death due to cardiac arrhythmia, especially VFib and may benefit from an ICD

12
Q

PVC couplet

A

2 successive PVCs

13
Q

PVC Bigeminy

A

Sinus beat followed by a PVC

14
Q

PVC Trigeminy

A

2 sinus eats followed by a PVC

15
Q

Atrial Fibrillation

A

multiple foci in atria fire continuously in chaotic pattern leading to Irregular, rapid ventricular rate

16
Q

In aFib the atrial rate is

A

> 400 bpm (most beats are inhibited at the AV node so the ventricular rate is about 75-175 bpm)

17
Q

aFib plus underlying heart disease equals marked increased risk of …

A

thromboembolism and hemodynamic compromise

18
Q

Signs and Symptoms of aFib

A

Fatigue and exertional dyspnea
Palpitations, dizziness, angina, syncope
Irregularly irregular pulse
thromboembolism

19
Q

How does aFib contribute to thromboembolic events?

A

Due to ineffective contraction, blood stasis occurs which leads to formation of intramural thrombi that can then embolize to brain

20
Q

ECG findings in aFib:

A

Irregular RR intervals with tiny erratic spikes with wavy baseline. No identifiable p waves.
Irregularly irregular rhythm

21
Q

Treatment for aFib in a hemodynamically unstable patient

A

Immediate electrical cardioversion to sinus rhythm

22
Q

Treatment of aFib in hemodynamically stable patient

A

Rate control (60-100 bpm) with Beta blocker or calcium channel blocker
Cardioversion (electrical preferred over pharm)
Anticoagulation to prevent embolic cerebrovascular accident

23
Q

What are choice pharmacologic agents for cardioversion?

A
Ibutilide
Procainamide
flecainide
sotalol
amiodarone
24
Q

why must a patient in aFib receive anticoagulation prior to cardioversion?

A

risk of embolization during cardioversion is significant, especially if aFib has been present for >48 hours

25
Q

How long should aFib patients be anticoagulated for?

A

3 weeks before cardioversion and 4 weeks after cardioversion

26
Q

What is the goal INR range for aFib patients?

A

INR of 2-3 is goal

27
Q

Treatment of chronic aFib includes

A

Beta Blocker or CCB for rate control

Anticoagulation with warfarin (unless under age 60 with lone-aFib)

28
Q

Cardioversion delivery

A

delivers shock in synchrony wiht QRS so that it does not hit T wave which could result in VFib

29
Q

Purpose of Cardioversion

A

terminate certain dysrhytmias like PSVT or VT

30
Q

Indications for cardioversion include:

A

aFib
Atrial flutter
VT with pulse
SVT

31
Q

defibrillation delivery

A

delivers shock that is not in synchrony with QRS complex

32
Q

purpose of defibrillation

A

convert dysrhythmia to normal sinus rhythm

33
Q

indications for defibrillation

A

VFib

VT without pulse

34
Q

indications for Automatic implantable defibrillator

A

VFib and/or VT not controlled by medial therapy

35
Q

atrial flutter pathophysiology

A

irritable automaticity focus in atria fires about 250-300 bpm leading to regular atrial contractions

AV node allows only 1 out of every 2-3 flutter waves to conduct to ventricles

36
Q

Causes of atrial flutter

A
HF (most common)
Rheumatic heart disease
CAD
COPD 
ASD
37
Q

Atrial flutter on ECG

A

saw tooth baseline
QRS every 2-3 teeth/p waves
Best seen in inferior leads ( II, III, aVF)

38
Q

Treatment for atrial flutter

A

rate control: beta blocker or CCB
restore NSR (cardioversion)
assess need for anticoagulatin

39
Q

Diagnosis of multifocal atrial tachycardia requires

A

at least three different p wave morphologies on ECG

40
Q

ECG finding in multifocal atrial tachycardia

A

variable p wave morphology

variable PR and RR intervals

41
Q

Multifocal atrial tachycardia usually occurs in patients with …

A

severe pulmonary disease (COPD)

42
Q

what has a similar diagnostic criteria to multifocal atrial tachycardia, except that HR is between 60-100 bpm (not tachycardic)?

A

Wandering Atrial Pacemaker

43
Q

Paroxysmal Supraventricular Tachycardia is most often due to….

A

Re-entry pathology:
AV nodal re-entrant tachycardia
Orthodromic AV re-entrant tachycardia

44
Q

What is the most common cause of supraventricular tachyarrhythmias

A

AV nodal re-entrant tachycardia

45
Q

What is AV nodal re-entrant tachycardia?

A

2 pathways are present within AV node; 1 fast, the other slow.

Re-entrant circuit is within AV node

46
Q

AV nodal re-entrant tachycardia is initiated and terminated by…

A

premature atrial complexes

47
Q

ECG with AV nodal re-entrant tachycardia

A

Narrow QRS with no discernible P waves

Circuit is short and conduction rapid leading to impulses exiting to activate atria and ventricle simultaneously, P wave is buried within the QRS

48
Q

What is orthodromic AV re-entrant tachycardia?

A

accessory pathway between the atria and ventricles that conducts retrogradely

49
Q

orthodromic AV re-entrant tachycardia is initiated or terminated by….

A

Premature atrial complexes or

premature ventricular complexes

50
Q

ECG with orthodromic AV re-entrant tachycardia

A

Narrow QRS complexes with P waves which may or may not be discernible depending on the rate

Accessory pathway is some distance from the AV node, thus re-entrant circuit is longer leading to a difference in timing of activation of atria and ventricles

51
Q

What is the most common arrhythmia associated with digoxin toxicity?

A

paroxysmal atrial tachycardia with 2:1 block

52
Q

Causes of paroxysmal supraventricular tachycardia

A

Ischemic heart disease
digoxin toxicity
AV node re-entry
atrial flutter with rapid ventricular response
AV reciprocating tachycardia (accessory pathway)
excessive caffeine or alcohol consumption

53
Q

What is the agent of choice for terminating SVTs?

A

IV adenosine (decreases SA and AV node activity)

54
Q

other agents that can be used for acute treatment of SVTs

A

Verapamil (CCB)
Esmolol (beta blocker)
digoxin

55
Q

what maneuvers help block re-entry mechanism in SVTs?

A

those that stimulate the vagus nerve that lead to a delay in AV conduction and blocks re-entry

Maneuvers include valsalva, carotid sinus massage, breath holding, head immersion in cold water

56
Q

side effects of adenosine

A
headaches
flushing
SOB
chest pressure
nausea
57
Q

Wolff-Parkinson-White syndrome:

A

accessory conduction pathway from atria to ventricles through bundle of Kent

causes premature ventricular excitation and may lead to paroxysmal tachycardia

58
Q

ECG with WPW syndrome:

A

Narrow complex tachycardia
Short PR interval
Delta wave: upward deflections seen before QRS

59
Q

Treatment for WPW syndrome:

A

radiofrequency catheter ablation of accessory pathway

Medical options: procainamide, quinidine

60
Q

which drugs should be avoided in WPW?

A

those that are active on the AV node: digoxin, verapamil, beta blockers

*these may accelerate conduction through accessory pathway

61
Q

which antiarrhythmics are better choices in WPW?

A

Type IA or IC antiarrhythmics

62
Q

define Ventricular tachycardia

A

rapid repetitive firing of three or more PVCs in a row at a rate of 100-250 bpm

AV dissociation is present
Originate below bundle of His

63
Q

sustained ventricular tachycardia

A

VT lasts longer than 30 seconds and is almost always symptomatic

*LIFE THREATENING arrhythmia that can progress to VFib if untreated

64
Q

Non-sustained VT

A

brief, self-limited runs of VT, that is usually asymptomatic

65
Q

what is associated with poor prognosis in VT?

A

If post-MI, especially if VT is sustained-VT

66
Q

Physical findings with VT

A

Cannon A Waves in the neck

S1 varies in intensity

67
Q

what arrhythmias account for most episodes of cardiac arrest?

A

VT and VFib causes 75% of cardiac arrests episodes

68
Q

Torsades de Pointes

A

Rapid polymorphic VT, that can often lead to VFib

Associated with prolongation of QT interval

69
Q

Treatment for Torsades de Pointes

A

IV magnesium provides cardiac stabilization

70
Q

Why is VT especially worrisome in patients with underlying heart disease and LV dysfunction?

A

These patients are at high-risk of sudden death

71
Q

VT on ECG

A

Wide and Bizarre QRS

QRS may be monomorphic or polymorphic

72
Q

Unlike PSVT, VT does not respond to ___________

A

Vagal Maneuvers or Adenosine

73
Q

Treatment of sustained VT in hemodynamically stable patients (BP >90):

A

ACLS recommends IV amiodarone, rocainamide, or sotalol

74
Q

Treatmnt of sustained VT in hemodynamically unstable patients:

A

Immediate synchronous DC conversion

Followed by IV amiodarone to maintain sinus rhythm

75
Q

All patients with sustained VT should undergo…..

A

placement of an ICD unless the ejection fraction is normal (then consider amiodarone)

76
Q

Treatment of nonsustained VT in patient with no underlying heart disease

A

Do NOT treat

*not at increased risk of sudden death

77
Q

Treatment of nonsustained VT in patients with underlying heart disease

A

order electrophysiologic study, if inducible, sustained VT consider ICD placement

Pharmacotherapy is second line (amiodarone has best results)

78
Q

What should be suspected in a patient with QRS tachycardia >0.12 second

A

Always suspect VT

79
Q

Cardiac Arrest

A

sudden loss of CO; potentially reversible if circulation and oxygen delivery are promptly restored

80
Q

Sudden Cardiac Death

A

unexpected death within one hour of symptom onset secondary to a cardiac cause

81
Q

Narrow complex tachycardias originate….

A

above the ventricles

82
Q

Wide complex tachycardias originate…

A

within the ventricles

*more ominous because more likely to progress to VFib

83
Q

Ventricular Fibrillation

A

Multiple Foci in ventricles fire rapidly, leading to chaotic quivering of the ventricles and no cardiac output

84
Q

Most episodes of VFib begin with…..

A

VT

85
Q

How is recurrence of VFib related to acute MI?

A

If VFib episode was NOT a/w acute MI, recurrence rate is high and chronic therapy is indicated.

If VFib develops within 48 hours of acute MI, recurrence rate is low

86
Q

Chronic therapy of VFib

A

prophylactic antiarrhythmic treatment with amiodarone or implantation of automatic defibrillator

87
Q

What is the most common cause of VFib?

A

Ischemic Heart Disease

88
Q

Clinical Features of VFib

A

Unconscious patient
cannot measure BP
Absent heart sounds and pulses

89
Q

VFib on ECG

A

no P waves
no QRS can be identified
Very irregular rhythm

90
Q

Treatment of VFib

A

immediate defibrillation and CPR: unsynchronized DC cardioversion (up to 3 sequential shocks)

If persistent: epinephrine every 3- minutes attemtp defibrillation again

91
Q

Treatment of refractory VFib

A

IV amiodarone followed by shock

Alternative second line: lidocaine, magnesium, procainamide

92
Q

What is the key to treatment of VFib?

A

Defibrillation!!!!
Also CPR and Epi

**Drugs cannot convert VFib by themselves

93
Q

Defibrillation does not work for….

A

asystole

perform CPR and administer Epi

94
Q

What is pulseless electrical activity? How do you treat?

A

Electrical activity on the monitor, but no pulses, even with doppler.

*grim prognosis

Treat the possible causes of asystole: hypoxia, hypovolemia, PE, tamponade, etc.

95
Q

Sinus Bradycardia

A

Sinus Rate

96
Q

Treatment for Sinus Bradycardia

A

Atropine can increase sinus rate by inhibiting vagal stimulation to the SA node

Cardiac Pacemaker if persistent

97
Q

Sick Sinus Syndrome

A

Sinus node dysfunction characterized by persistent spontaneous sinus bradycardia

Usually Elderly

98
Q
First Degree AV Block:
PR interval?
QRS?
Delay location?
Treatment?
A

PR interval prolonged: >0.20 second
QRS follows each P wave
Delay usually in AV node
Benign, no treatment required

99
Q

What are the second degree AV block types?

A

Mobitz Type I = Wenckebach

Mobitz Type II

100
Q

Which AV blocks require pacemaker implantation?

A

second degree AV block Mobitz type II

3rd degree AV block

101
Q

2nd degree AV block Mobitz Type I

A

progressive prolongation of PR interval until P wave fails to conduct

Site of block usually in AV node

Benign, no treatment required

102
Q

2nd degree AV block Mobitz Type II

A

P wave fails to conduct suddenly without preceding PR prolongation
QRS also drops suddenly
Often leads to complete heart block (3rd degree)
Site of block is within the His-Purkinje system

103
Q

3rd degree AV block (complete heart block)

A

Absence of conduction of atrial impulses to ventricles

There is no correspondence between P waves and QRS

AV dissociation
Ventricular Rate of 25-40 bpm