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cardiology exam iii > Cardio 27 : Supraventricular Tachyarrhythmias > Flashcards

Cardio 27 : Supraventricular Tachyarrhythmias Flashcards

1
Q

Supraventricular

A

Rhythm generated above the ventricles

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2
Q

Tachyarrhythmia

A

Atrial complexes greater than 100 bpm

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3
Q

Supraventricular Tachyarrhythmia

A

Abnormal action potential (impulse) formation by SA node, atria or junction/AV node

OR

Abnormal conduction of impulses through normal or abnormal pathways

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4
Q

What part of the conduction system is mostly responsible for ventricular responses in SVT ?

A

AV node

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5
Q

What drugs can be given to help slow AV nodal conduction ?

A

Adenosine
BB’s
CCB’s (Non DHP’s -Verapamil and Diltiazem)
Dihydropyridines have vasodilatory effect. Little
effect on chronotropy
Digoxin

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6
Q

3 Electrophysical etiologies for SVT

A

Tissue automaticity
Triggered Activity
Re-entry

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7
Q

Tissue automaticity (etiology)

A

Foci in cardiac tissues become more “irritable”-more likely to cause their own action potential

Usually seen in setting of systemic stress or from a biochemical effect on tissues

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8
Q

What is the state of the ANS in increased tissue automaticity ?

A

Increased Sympathetics
Decreased PS.

Other factors leading to automaticity include:
Increased systemic catecholamines
Hypoxemia
Hyperthyroidism
Chemical stimulants, including caffeine
Drugs-excess Digoxin, toxins (ethanol)
Stretch of myocardium
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9
Q

Re-entry SVT is due to …

A

two adjacent areas of conducting tissue with differing conduction velocities and refractory periods. Abnormal conduction between them sets off a circuit that rapidly paces the atria and/or the ventricles.

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10
Q

The timing of Re-entry SVT tends to be

A

paroxysmal and short lived

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11
Q

Triggered SVT

A

An action potential (depolarization) that occurs during the repolarization period of a preceding AP

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12
Q

paroxysmal

A

term applied to several types of tachycardias, essentially means rapid onset, and often rapid termination.

NOT GRADUAL

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13
Q

Symptoms of SVT

A 
Palpitations
Fatigue
Lightheadedness
Chest discomfort
Dyspnea
Presyncope
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14
Q

What symptom rarely occurs with SVT

A

syncope

More associated with :
Abrupt termination of SVT
Other structural abnormalities 
    Aortic stenosis, hypertrophic cardiomyopathy,
    etc.
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15
Q

palpitations that are Nonparoxysmal with gradual onset and termination are indicative of …

A

Physiologic Sinus Tachycardia

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16
Q

palpatations that are Irregular are associated with..

A

Premature complexes, Atrial Fibrillation, or Multifocal Atrial Tachycardia

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17
Q

Palpitations that are Recurrent with abrupt onset and termination are indicative of

A

paroxysmal (very likely re-entry SVT)

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18
Q

Palpitation that can be terminated by vagal maneuvers likely involve

A

Re-entry involving AV node

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19
Q

Persistant tachycardia of weeks- months duration can cause what dangerous morbidity to occur ?

A

cardiomyopathy and subsequent heart failure if not treated

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20
Q

List the different types of SVT

A 
Sinus tachycardia
AV Nodal Re-entry
Junctional tachycardia
Atrial Tachycardia
Multifocal Atrial Tachycardia
Atrial Fibrillation
Atrial Flutter
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21
Q

sinus tachycardia

A

Tachycardia with impulses originating from the sinus node.

Can be due to increased automaticity of sinus node, can also be re-entrant.

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22
Q

Types of sinus Tachycardia

A

Physiologic Sinus Tachycardia
Inappropriate Sinus Tachycardia
Postural Orthostatic Sinus Tachycardia (POTS)
Sinus Re-entry

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23
Q

An expected increase in sinus rate above 100 BPM due to a given level of physical, emotional, pathological or pharmocologic stress.

A

Physilogic stress

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24
Q

Causes of physiologic stress

A

Physical/Emotional: Exercise, fear, anger, stress, etc.
Pathologic: fever, anemia, MI, hypoxia, hypovolemia, CHF, pulmonary embolism, infection, shock, thyrotoxicosis, pheochromocytoma
Pharmocologic:
1.Stimulants: caffeine, nicotine, alcohol, amphetamines, cocaine, ectasy, other recreational drugs
2.Prescribed medications: Beta agonists, atropine, aminophylline, catecholamines, some anti-cancer drugs

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25
Q

EKG findings of Physiologic Sinus tach

A

(+) P-waves in I, II, aVF (Left sided leads), (-) in aVR

Normal PR interval
P waves may become peaked, have large amplitude
Every P-wave associated with a QRS complex, except in setting of AV block

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26
Q

What is the main goal of treating physiologic sinus tach ?

A

Treat the underlying cause !

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27
Q

Beta Blockers are used to treat physiologic sinus tach. under what conditions

A

emotion/anxiety related disorders
MI, CHF
Thyrotoxicosis (diltiazem or verapamil if beta blocker is C/I)

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28
Q

Inappropriate sinus tach

A

Persistent increase in sinus rate out of proportion to or without physical, emotional, pathological or pharmocologic stress.

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29
Q

What is likely the cause of Inappropriate sinus tach

A

Mechanism likely due to enhanced automaticity or abnormal excess sympathetic or reduced parasympathetic tone.

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30
Q

Criteria for diagnosing sinus tach

A

Persistent sinus tach during the day with excessive increase in rate in response to activity, with normalization of heart rate at night

Tachycardia and symptoms are not paroxysmal
P-wave morphology identical with sinus

Exclusion of other causes (anemia, hyperthyroidism, etc.)

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31
Q

Beta blockers are first line for symptomatic pts with Innapropriate Sinus tach. What can be done if patient is refractory to this ?

A

Ablation therapy

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32
Q

POTS

A

Syndrome of excessive tachycardia that is induced by standing up and relieved by lying down.

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33
Q

Mechanism for POTS formation

A

Central beta-hypersensitivity of baroreflex that does not terminate tachycardia induced by standing upright

Mild peripheral autonomic neuropathy that impairs appropriate vasoconstriction o standing.

Presence of autoantibodies to autonomic neurotransmitter receptors-one half of POTS cases are seen in setting of preceding viral illness
Others, not all mechanisms are known or understood

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34
Q

DIagnosis of POTS

A

1) EKG showing sinus tachycardia
2) Head upright tilt table test showing increase in at least 30 bpm, or rate greater than 120 after 5-10 minutes upright
3) Absence of orthostatic hypotension
4) Absence of known autonomic neuropathy
5) Symptoms provoked by standing upright, relieved by lying down

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35
Q

Non-pharmacologic tx includes :

A

Volume expansion is mainstay-copious fluid and salt intake
Thigh high compression stockings
Sleeping with head of bed elevated (increases vasopressin secretion)

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36
Q

Sinus Node Re-entry Tachycardia

A

Paroxysmal episodes of sinus tach, usually triggered by and terminated by an ectopic atrial beat

Unknown whether re-entry circuit is confined to sinus node or includes near-by tissue, but usually responds to vagal maneuvers and adenosine, so likely that sinus node is involved in a re-entry circuit

37
Q

Sinus Node Re-entry Tachycardia Diagnosis:

A

1) Tachycardia and symptoms are paroxysmal
2) P-wave morphology identical to sinus
3) Rhythm induced and/or activated by premature atrial stimuli
4) Termination occurs with vagal maneuvers or adenosine
5) Induction of rhythm does not depend on atrial or AV nodal conduction time
6) EP Study is definitive

38
Q

Treatment of SNRET

A

adenosine, vagal maneuvers, amiodarone, beta-blockers, verapamil, diltiazem or digoxin.
Refractory cases may need EP study with ablation.

39
Q

Atrioventricular Nodal Reciprocating Tachycardia

A

Most common cause of paroxysmal SVT

May involve AV nodal tissue only or AV node and nearby atrial tissue.

40
Q

Re-Entry mechanism

A

A re-entry circuit is set up in the setting of a ectopic beat occurring after a normally conducted impulse-one pathway is refractory and therefore blocked, while the other conducts the beat. The blocked pathway then repolarizes and “catches” the returning depolarization, sending it back up the circuit and causing a re-entry circuit.

41
Q

Typical AVNRT

A

The slow pathway conducts the impulse from the atria to the ventricles, therefore the slow pathway is the antegrade pathway.

results in a p-wave that is during or close to the QRS. This is called a short RP interval (≤ 70 msec,short). The P-wave is also short (40 msec). The p-wave sometimes produces a pseudo-r’.

42
Q

Atypical AVNRT

A

Fast pathway is antegrade, producing a long RP interval.

43
Q

Dx of AVNRT

A

Dx is best ascertained by intra-cardiac EP.

44
Q

EKG of Typical AVNRT

A

HR 140-250 BPM

short RP interval (less than 70 msec), short p-wave (40 msec) pseudo-r’ in lead V1.

45
Q

EKG of Atypical AVNRT

A

long RP interval, p-wave negative in leads III, aVF and is inscribed before the QRS complex.

Inverted p-wave (junctional)

46
Q

treatment of acute ustable AVNRT

A

Direct current CVN

47
Q

Treatment of acute stable AVNRT

A

adenosine, vagal maneuvers

48
Q

Long Term treatment of AVNRT

A

either pharm or ablation

Ablation of slow conduction is definitely more effective in the long run

Risk of ablation includes heart block and subsequent need for pacemaker implantation.

49
Q

Junctional Tach.

A

Tachycardia originating in junctional region between AV node and His-Purkinjie system

50
Q

Focal Junctional Tach

A

Very uncommon
Paroxysmal
Originates from AV node or Bundle of His
Due to increased automaticity or triggered phenomena
Usually presents in pediatric ages or young adulthood**
Pts quite symptomatic, can go into heart failure if tachycardia is incessant**

51
Q

Diagnosis of Focal Junctional Tach.

A 
HR 110-250 bpm
Narrow complex or BBB pattern
AV dissociation often present
Rhythm may sometimes be erratic, like Atrial fibrillation
Best demonstrated by EP study
52
Q

Tx of Focal junctional block

A

Beta Blockers are good pharmcologics.

Ablation may be needed but may have risk of AV block

53
Q

Non Paroxysmal Junctional Tach.

A

Benign arrhythmia**
Due to enhanced automaticity or triggered mechanism
Gradual onset and termination-”warm up and cool down”
Can not be terminated by pacing maneuvers**
HR usually 70-120 bpm

54
Q

What may Non Paroxysmal Junctional Tach. be a marker for ?

A 
Digitalis Toxicity
Hypokalemia
Myocardial Ischemia
After cardiac surgery
COPD
Hypoxia
Inflammatory conditions
55
Q

Tx of COPD Non Paroxysmal Junctional Tach.

A

BB’s

Mainly just treat the underlying cause !

56
Q

AVRT differs from AVNRT in that …

A

Tachycardia reciprocating between atria and ventricles by using extranodal accessory pathways

Accessory pathways are conductive tissue bridges that cross the insulating fibrous valvular annulus

57
Q

What is unusual of accessory pathways ?

A

Accessory pathways can be capable of antegrade or retrograde conduction of APs

58
Q

What occurs if accessory pathway is anterograde

A

If accessory pathway conduction is antegrade, the QRS will be skewed slightly at the beginning, the so-called Delta wave. This phenomenon is called “pre-excitation”

59
Q

If accessory pathway conduction is retrograde

A

then the pathway is called “concealed”, because the initial impulse conducts normally down the AV node and is not evident on EKG tracing.

60
Q

Pre-excitation (delta wave + normal rhythm) + tachyarrhythmia =

A

Wolff-Parkinson-White Syndrome

61
Q

Orthodromic AVRT

A

the impulse travels antegrade down AV node and retrograde up accessory pathway

Majority of AVRT

62
Q

Antidromic AVRT

A

impulse travels antegrade down accessory pathway and retrograde up AV node

63
Q

QRS complex of orthodromic AVRT ?

A

Orthodromic AVRT will usually yield a narrow complex tachycardia, outside of the setting of aberrancy or bundle branch block

64
Q

QRS complex of antidromic AVRT

A

Anti-dromic AVRT usually results in a wide complex tachycardia

65
Q

Most common arrhythmia with Wolff Parkinson White ?

A

AVRT is most common arrhythmia (95%)

66
Q

In patients with WPW and A-Fib, accessory pathways seem to play a role in causing the A-Fib. What can be done to correct this ?

A

Abblation !

67
Q

Of note, A-Fib in the setting of young, healthy people is strongly associated with

A

pre-excitation. That is to say,

68
Q

what is the recommended treatment for WPW

A

for WPW that is diagnosed, catheter ablation is strongly recommended due to the risk for degeneration to A-Fib and sudden death.

69
Q

What is the treatment of choice for a patient with hemodynamically stable AVRT

A

Ibutilide, procainamide, or flecainide are the treatments of choice medically due to their conduction slowing properties.

Adenosine must be given judiciously

70
Q

atrial tach.

A

Tachycardia resulting from impulse formation in atrial focus not related to sinus node or AV node

71
Q

Focal atrial Tach.

A

Paroxysmal OR Gradual onset/termination
HR 100-250, rarely 300
Benign except in incessant forms

Can be caused by increased automaticity, re-entry, or triggered mechanisms. **

72
Q

Drug induced focal atrial tachy.

A

Digitalis toxicity can induce a focal atrial tachycardia with a slow ventricular response (due to digoxin induced AV block)

Treatment is holding digoxin, administration of digoxin antibodies if heart block continues

73
Q

why is it important to figure out the direct cause of FAT (re-entry, automaticity, triggered)

A

*Specific medicinal therapy depends on whether FAT is due automaticity, re-entry, etc.

74
Q

TOC for unstable FAT

A

: Cardioversion

75
Q

TOC for Acute, hemodynamically stable pt with FAT

A

adenosine, beta blockers, central calcium channel blockers, flecainide, propafenone, amiodarone, sotalol

76
Q

TOC for Recurrent Symptomatic/incessant FAT

A

catheter ablation

77
Q

Multifocal Atrial Tachycardia

A

Atrial Tachycardia with three or more sites of impulse generation
P waves will have multiple shapes Irregular rhythm!
Irregular sensation of palpitations
Almost always associated with pulmonary disease, metabolic disease, or electrolyte imbalance *****

78
Q

treatment of MFAT

A

Treat the underlying disease state!
Almost always associated with pulmonary
disease, metabolic disease, or electrolyte
imbalance *****

Rate control usually with calcium channel blockers, Beta blockers often C/I due to lung disease

79
Q

Atrial flutter

A

Also called “macro-re-entrant atrial tachycardia”
Organized atrial rate between 250-350 bpm
Ventricular rates may be 2:1, 3:1, etc, or variable
Atrial rhythm shows regular, frequent p-waves on EKG called “flutter waves”

80
Q

Etiology of atrial flutter

A 
Due to re-entry circuits set up around: 
Cavotricuspid isthmus (CTI)
Area of prior scarring in atria
81
Q

Cavotricuspid isthmus (CTI) dependant Atrial Flutter

A

Most common cause for Atrial Flutter
Re-entry circuit most often propagates counterclockwise around tricuspid valve
Can also be clockwise, or involve other patterns around cavotricuspid isthmus, but these are rare

82
Q

Cavotricuspid isthmus independant Atrial Flutter

A

Most atrial flutter not involving the cavotricuspid isthmus is found involving areas of prior scarring of the atria, usually from cardiac surgery
Also called “lesion related macro-re-entrant atrial tachycardia”
Usually flutter waves on EKG are less well demonstrated

83
Q

Unstable atrial flutter

A

Cardioversion (CVN) and/or rate control with BBs, Verap, Dilt, Dig, Amio

84
Q

Stable atrial flutter

A

Atrial overdrive pacing, DC CVN, ibutilide, flecainide, propafenone, sotalol, procainamide, amio

85
Q

Treatment of long term atrial flutter

A

Overall direct current cardioversion of first episode and catheter ablation of recurring atrial flutter are very successful. Pharmacologic cardioversion is not, and carries inherant risks of anti-arrhythmic drugs.

86
Q

why will you not cardiovert a patient with Atrial flutter ?

A

Studies have shown a risk for thrombo-embolism after DC CVN of Atrial flutter. Attempts to convert to sinus rhythm should only occur if:
Patient is anti-coagulated to INR of 2-3
Arrhythmia is less than 48 hours old
TEE shows no clots (anti-coagulate anyway)

87
Q

waht is a major danger associated with atrial fibrillation ?

A

As atria have no organized contractile ability, blood movement is poor. Static blood may form clots that can embolize

88
Q

unstable atrial fibrillation

A

Cardioversion !

89
Q

Stable

A

Rate control with BB’s etc

cardiology exam iii (12 decks)

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