Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Cardio > Arrhythmias > Flashcards

Arrhythmias Flashcards

1
Q

What causes an arrhythmia?

A

interruption of the sinus impulse or the sequence of conduction through the heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the 3 kinds of arrhythmias?

A

Arrhythmias can be benign, asymptomatic, or life-threatening

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the conduction pathway?

A
  1. Sinoatrial node
  2. Atroventricular node
  3. Bundle of His
    Bundle branch, fascicle, ventricle
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Which cells have intrinsic automaticity?

A

Cells that normally have this ability are in the cardiac specialized conduction system:
–Sinoatrial (SA) node
–Atrioventricular (AV) node
–His-Purkinje system (pacemaker cells)
If automatic rate is higher than SA node rate, then ectopic beats/rhythm results

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the myocyte action potentials?

A
  1. Na+ in - straight line up (+)
  2. K+ and Cl- out - small dip
  3. Ca2+ in and K+ out - plateau
  4. K+ out - full depolarization
  5. K+ - plateau
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is normal sinus rhythm?

A

Implies normal sequence of conduction, originating in the sinus node and proceeding to the ventricles via the AV node and His-Purkinje system.
EKG Characteristics:
Rate 60-100 bpm
Regular rhythm
Each QRS complex is preceded by a P wave and vice versa
P wave is upright in lead II & downgoing in lead aVR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the phases of pacemaker action potential?

A

Phase 0: Ca2+ in
Phase 3: K+ out
Phase 4: Na+ and Ca2+ in

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What does beta-adrenergic stimulation do?

A

steeper Phase 4 slope, shifts action potential threshold more negatively (more open Ca++)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What does parasympathetic stimulation do?

A

vagus nerve decreases open If (Na+), causing flatter Phase 4 slope; shifts action potential threshold voltage more positively (less open Ca++)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is triggered activity and how does it differ from automaticity?

A

Under certain conditions (such as prolonged repolarization), one abnormally depolarized action potential can trigger subsequent depolarizations (called afterdepolarizations).; Differs from automaticity because afterdepolarizations are not spontaneous but instead require a prior action potential to stimulate (hence the term “triggered” activity).; If afterdepolarizations reach threshold voltage, can result in ectopic beats or tachyarrhythmias.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are early afterdepolarizations?

A

Augmentation in inward Ca++ (if during Phase 2) or Na+ channels (if during Phase 3). Usually occur in the setting of prolonged repolarization, causing depolarization if reaches membrane threshold.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are examples of early afterdepolarizations?

A

Long QT syndrome, Torsades des Pointes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are delayed afterdepolarizations?

A

Augmentation in a Ca++ channels in Phase 4, causing depolarization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are examples of delayed afterdepolarizations?

A

Clinical scenario: digoxin toxicity (secondary to elevated intracellular Ca++ that is released from cells) or catecholamine stimulation.
Arrhythmia: bidirectional/ idiopathic VT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is a conduction block?

A

Occurs when impulse reaches electrically unexcitable area; Block could be transient vs. permanent, bidirectional vs. unidirectional; Complete conduction block can lead to bradyarrhythmias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What can cause altered impulse conduction?

A

Ischemia, fibrosis, drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What promotes re-entrant arrhythmias?

A

Decreased conduction velocity: Partially depolarized tissue with inactivated sodium channels- myocardial ischemia, Scarring, disruption of architecture- chronic MI, Remodeling/redistribution of connexins- cardiomyopathies; Heterogenous refractoriness: Myocardial ischemia/infarction, Inflammation, Cardiomyopathies, Electrolyte abnormalities/drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What kinds of acquired structural heart disease promote arrhythmias?

A 
A.Acute myocardial infarction
B.Chronic ischemic heart disease
C.Hypertensive heart disease
D.Dilated non-ischemic cardiomyopathy
E.Infiltrative cardiomyopathy
F.Cardiac sarcoidoses
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What kinds of congenital structural heart disease promote arrhythmias?

A

A.Hypertrophic cardiomyopathies
B.Congenital dilated cardiomyopathies
C.Arrhythmogenic right ventricular dysplasia
D.Anomalous coronary arteries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How do long and short QT syndrome affect arrhythmias?

A

potassium or sodium channelopathies resulting in abnormal repolarization and propensity to polymorphic VT (Torsades des Pointes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is sinus tachycardia? What causes it?

A

Occurs when sinus rhythm increases above 100 bpm; Caused by fever, hyperthyroidism, volume depletion, anxiety, sepsis, etc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is Premature Atrial Complex?

A
  • P wave from another atrial focus
  • Occurs earlier in cycle
  • Different morphology of p wave
  • Benign, common cause of perceived irregular rhythm
  • Can cause symptoms such as: skipped beats, palpitations
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is Atrioventricular Nodal Tachycardia?

A

reentrant loop - a little conduction block down one limb, but come around on second pass - two pathways (“fast” and “slow”); Usually symptomatic with abrupt onset/offset of regular palpitations; causes simultaneous atrial and ventricular activation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is Atrioventricular Reentry Tachycardia?

A

Accessory Pathway or Bypass Tract - not going through normal electrical conducting fibers - going
through ventricles on cell-to-cell basis (this is slower than
going through electrically insulated conduction tissue)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is seen on EKG when Atrioventricular Reentry Tachycardia occurs?

A

Delta wave (slurring of QRS), Shortened PR, Widened QRS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is Wolff-Parkinson-White Syndrome?

A

Atrioventricular Reentry Tachycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is Focal Atrial Tachycardia?

A

single site of origin a tach

28
Q

What is Multifocal Atrial Tachycardia?

A

multiple (3+) sites of origin

29
Q

What is atrial fibrillation?

A

SVT marked by rapid (350+ bpm), irregular and disorganized atrial activity (i.e., no discrete p-waves!); Ventricular rate is irregular; most common sustained arrhythmia seen in clinical practice

30
Q

What causes a fib?

A 
Altered atrial anatomy/physiology
•Fibrosis (age or myopathy-related)
•Inflammation – e.g., pericarditis
•Enlarged atrial size – e.g., concomitant valvular disease
–Altered atrial refractoriness (i.e, shorter)
•Hyperthyroidism
•Alcohol, stimulants
•Vagal tone
31
Q

What is atrial flutter?

A

Macroreentrant circuit, usually originating in right atrium and revolving around the tricuspid valve (approximately 300 bpm).

32
Q

What is a junctional rhythm?

A

Characterized by lack of p-waves; Due to increased automaticity of AV node junction over Sinus node; Junctional Rhythm is typically 40-60 bpm (automatic rhythm of AV node)

33
Q

What are common etiologies of junctional rhythm?

A
  • Digoxin toxicity
  • Beta-agonists, e.g. isoproterenol
  • Myocardial ischemia
  • Myocarditis
  • Cardiac surgery
  • Anything that decreases sinus node automaticity: e.g., beta-blockers
34
Q

Which supraventricular tachycardias have irregular ventricular rates?

A
  • Multifocal Atrial Tachycardia
  • Atrial Fibrillation
  • Atrial Flutter/variable AV Block
  • Atrial Tachycardia/variable AV Block
35
Q

Which supraventricular tachycardias have regular ventricular rates and p waves?

A
  • Sinus Tachycardia
  • Atrial Tachycardia
  • Atrial Flutter
  • some AVNRT/AVRT
36
Q

Which supraventricular tachycardias have regular ventricular rates and no p waves?

A
  • Junctional Tachycardia

- AVNRT

37
Q

What is Premature Ventricular Complex?

A

bizarre widened beat that occurs before it should; Extremely common throughout the population, both with and without heart disease; Usually asymptomatic, except rarely dizziness or fatigue in patients that have frequent PVCs and significant LV dysfunction

38
Q

What is non-sustained ventricular tachycardia?

A

3 or more consecutive ventricular beats with rate 100+ bpm, lasting less than 30 seconds

39
Q

What is sustained ventricular tachycardia?

A

consecutive ventricular beats with rate 100+ bpm, lasting more than 30 seconds

40
Q

What are Torsades des Pointes?

A

Polymorphic VT in the setting of long QT interval

41
Q

What is Ventricular Fibrillation?

A

Chaotic, disorganized ventricular rhythm; like a fib in that the ventricles are being depolarized in a totally chaotic manner, but unlike a fib, this is a lethal state if it is perpetuated b/c the ventricles can’t sustain CO @ 300 bpm

42
Q

What are causes of sinus bradycardia?

A
  • Normal aging
  • 15-25% Acute MI, esp. affecting inferior wall- often resolves
  • Hypothyroidism, infiltrative diseases (sarcoid, amyloid)
  • Hypothermia, hypokalemia
  • Collagen vascular diseases
  • Situational: micturation, coughing
  • Drugs: beta-blockers, digitalis, calcium channel blockers, amiodarone, lithium
43
Q

What is 1st Degree AV block?

A

PR interval 200+ms; If accompanied by wide QRS, refer to cardiology secondary to risk of progression to higher-degree block (ventricle may also be diseased); Otherwise, benign if asymptomatic

44
Q

What is 2nd Degree AV Block Mobitz type I (Wenckebach)?

A

Progressive PR prolongation, with eventual non-conduction of a p wave; Usually asymptomatic; Can be caused by drugs that slow conduction (beta blockers, calcium channel blockers, digoxin); Can be corrected if reversible cause- e.g., avoid meds that block conduction; Can cause angina, syncope (esp. in elderly), leading to requiring a Pacemaker

45
Q

What is 2nd degree block Type II (Mobitz 2)?

A

Normal PR intervals with sudden failure of a p wave to conduct; Usually below AV node and accompanied by BBB or fascicular block; Often causes pre/syncope; exercise worsens symptoms; Treat with pacemaker

46
Q

What is 3rd Degree AV Block?

A

Complete AV dissociation with atrial rate faster than ventricular rate; Will often be symptomatic- dizziness, syncope, angina, heart failure

47
Q

What are the 3 strategies of antiarrhythmic agents?

A

1.Decrease automaticity - Decrease Phase 4 slope
2.Change conduction velocity - Decrease Phase 0 slope
(and Phase 4)
3.Change refractory period - Prolong Phase 2 & Phase 3

48
Q

Which drugs slow automaticity?

A

Beta and calcium blockers

49
Q

Which drugs change refractoriness or conduction velocity?

A

Potassium and sodium blockers

50
Q

What is the Vaughan Williams Classification?

A 
•Class I: sodium channel blockers
–Inhibit depolarization/slow conduction velocity
•Class II: beta-blockers
–Slow sinus node and AV node
•Class III: potassium channel blockers
–Prolong repolarization
•Class IV: calcium-channel blockers
–Slow SA node (some) and AV node (more)
51
Q

What do Class I drugs do?

A

Sodium Channel Blockers

  • Decrease slope of Phase 4
  • Decrease slope of Phase 0
  • IA & IC prolong repolarization and IB shortens repolarization
52
Q

What are the 3 kinds of Class I drugs?

A

IA: moderate decrease in slope
IB: mild decrease
IC: marked decrease

53
Q

What are Class IA drugs?

A

Class IA agents: quinidine, procainamide, disopyramide
–Increase action potential duration – watch QT
–Caution in renal dysfunction

54
Q

When are Class IA drugs used?

A

SVTs, AF, VT; Use has declined because of more effective/less proarrhythmic meds

55
Q

What are Class IB drugs?

A

Class IB agents: lidocaine (IV), mexiletine (oral), phenytoin (rarely used)
–Use-dependent: better effect at faster heart rates secondary to affinity for open Na channels
•Little effect on atrial tissue: atrial cells have a shorter action potential duration; less time for drug to bind to activated Na channels. Large effect on diseased/ischemic ventricular tissue
–Reduce action potential duration (block Na channels that persist through phase 2)
•Do not increase QT, so can be used for afterdepolarizations (e.g., digoxin-induced VT and torsades de pointes/long QT)
–Caution in hepatic dysfunction

56
Q

When are Class IB drugs used?

A

VT (doesn’t work well in atrial cells)

57
Q

What are Class IC drugs?

A

Type IC agents: flecainide, propafenone
–Slower kinetics, affinity for activated sodium channel
–Most potent sodium blocking effect, and therefore largest effect on ECG (even at rest secondary to slower kinetics): watch for widening of the QRS

58
Q

When are Class IC drugs used?

A

AF, refractory SVTs; dangerous to use in patients with structural heart disease

59
Q

What is the dangerous side effect of Class IC drugs?

A

Pro-arrhythmic!!!!!
•Increased mortality in patients with structural heart disease (e.g., post-myocardial infarction)
•Can slow atrial flutter rates and cause 1:1 AV conduction – use with AV node blockers

60
Q

What are Class II drugs?

A

Beta-adrenergic Blockers; Class II agents: metoprolol, propranolol, esmolol, etc…
Class II mechanisms: block cardiac beta-1 adrenergic receptors
–Slow sinus rate
–Prolong A-V node conduction and refractoriness
–Inhibit automaticity
–Block effect of catecholamines

61
Q

When are Class II drugs used?

A

–Useful for SVTs and VT (esp. exercise- or emotionally-induced)
–Controls ventricular rate in AF/FL
–Mortality benefit in MI and CHF patients

62
Q

What are Class III drugs?

A

Class III: Potassium Channel Blockers
Class III agents: amiodarone, sotalol, dofetilide, ibutilide (IV), dronedarone
Class III mechanisms: block cardiac potassium channels (phase 3)
–Prolong refractoriness/QT
–Amiodarone also: Decreases conduction velocity (phase 0) and automaticity (phase 4)

63
Q

When are Class III drugs used?

A

Atrial fibrillation, VT

64
Q

What are the dangerous side effects of Class III drugs?

A

Long QT/Torsades, Reverse-use dependence (Greater drug effect at slower heart rate, causing more tissue refractoriness/long QT/Torsades at slower heart rates); May be better at preventing arrhythmias than stopping them

65
Q

What is Amiodarone?

A

Features of all 4 Vaughan Williams classes; Most effective drug for preventing recurrent AF and for VT/VF – particularly in cardiomyopathy patients, where other drugs can be more proarrhythmic; adverse events are in basically every organ system

66
Q

What are Class IV drugs?

A

Class IV agents: diltiazem and verapamil
Class IV mechanism: block L-type calcium channels (Phase 4 & 0)
–Clinical effects
•Prolonged AV node conduction and refractoriness
•Sinus node slowing (mild)
•Reduce automaticity (mild)
•Use-dependent properties

67
Q

When are Class IV drugs used?

A

Rate control for AF/AFL, treatment of SVT

Cardio (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions