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Cardiology > Cards Test 1 Combo > Flashcards

Cards Test 1 Combo Flashcards

1
Q

Arrhythmia commonly found in COPD/lung disease patients

A

Multifocal Atrial Tachycardia

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2
Q

continuous rapid-firing of multiple atrial automaticity foci

A

atrial fibrillation

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3
Q

What should you think if you have a ventricular rate of exactly 150bpm?

A

atrial flutter

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4
Q

Which BBB can be fairly common in healthy hearts?

A

Right BBB

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5
Q

Which leads are useful in assessing atrial enlargement?

A

V1 and II

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6
Q

Why is V1 useful in assessing atrial enlargement?

A

it’s perpendicular to the flow of electricity through the atria, and thus produces a nice biphasic P wave that’s useful to look at when left atrial enlargement is suspected

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7
Q

Why is lead II useful in assessing atrial enlargement?

A

Lead II is parallel to the flow of electricity in the atria, and will thus be enlarged if atria are enlarged

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8
Q

Evidence of RAE on EKG?

A

-P wave > 2.5mm in leads II or the first part of the diphasic P wave in V1

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9
Q

Evidence of LAE on EKG?

A
  • terminal portion of the diphasic P wave in V1 should drop at least 1 mm below the isoelectric line
  • or the terminal portion should be at least 0.04sec in width
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10
Q

Why is LAE sometimes called P mitrale?

A

-because mitral valve disease is the most common cause

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11
Q

Why is RAE sometimes called P pulmonale?

A

-because it’s often caused by severe lung disease

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12
Q

Evidence of right ventricular hypertrophy on EKG?

A

-large R wave in V1 (normally the S wave is larger)

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13
Q

Evidence of left ventricular hypertrophy on EKG?

A

-S wave in V1 + R wave in V5 > 35mm

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14
Q

Only in what type of patient is it safe to diagnose RVH? Why?

A
  • patient with lung disease

- because lung disease with it’s associated RV afterload increase should be the only real reason for RVH

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15
Q

Triad of myocardial infarction

A
  • ischemia
  • injury
  • necrosis
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16
Q

Evidence of ischemia on EKG

A
  • ST depression

- T wave inversion

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17
Q

What is ST elevation on EKG?

A

infarction

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18
Q

Evidence of infarction on EKG?

A

-ST elevation

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19
Q

What is ST depression on EKG?

A

ischemia

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20
Q

What are the three stages through which an EKG evolves during an acute myocardial infarction?

A
  • T wave peaking followed by T wave inversion
  • ST segment elevation
  • Appearance of new Q waves
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21
Q

In what lead(s) is T wave inversion normal

A

-V1

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22
Q

In which leads would T wave inversion be present in a patient with Wellens Syndrome?

A

V2 and V3

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23
Q

What is the worst “kind” of ST depression?

A
  • downsloping

- horizontal is also bad

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24
Q

What makes a Q wave significant?

A
  • at least 0.04 seconds (1 small square) wide

- or 1/4 of the entire QRS amplitude

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25
Q

What do significant Q waves indicate?

A

irreversible myocardial cell death

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26
Q

How does hypocalcemia manifest on EKG? Why?

A
  • prolonged QT interval

- because this is where ventricular contraction occurs, and not enough calcium prolongs ventricular contraction

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27
Q

What arrhythmia may be triggered by hypocalcemia?

A

-Torsades de pointes

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28
Q

possible causes of hypocalcemia

A
  • primary/secondary hypoparathyroidism
  • vitamin D deficiency
  • chronic kidney disease
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29
Q

How does hypercalcemia manifest on EKG? Why?

A
  • shortened QT interval

- b/c a lot of calcium allows for very quick ventricular contraction

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30
Q

Possible causes of hypercalcemia

A
  • malignancy
  • chronic kidney disease
  • adrenal insuffiency
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31
Q

How does hypokalemia manifest on EKG? Why?

A
  • Early: T wave flattening
  • ST segment starts to depress and can invert the T wave
  • U wave in severe cases
  • Remember that K+ is involved in phase 3 repolarization, which manifests on the T wave of EKG
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32
Q

causes of hypokalemia

A
  • diuretics

- vomiting/diarrhea

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33
Q

How does hyperkalemia manifest on EKG? Why?

A
  • peaked T waves
  • P waves may be flattened or absent
  • Severe: QRS widens and fuses with T wave
  • remember that K+ is involved in phase 3 repolarization, which manifests on the T wave of EKG
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34
Q

Causes of hyperkalemia

A
  • ACE inhibitors
  • K+ sparing diuretics
  • renal failure
  • hypoaldosteronism
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35
Q

Normal PR interval

A

0.12-0.20

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36
Q

what should you think if there’s a lengthened PR interval?

A

AV block

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37
Q

what should you think if there’s a shortened PR interval?

A

accessory pathway

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38
Q

What is the normal duration of the QRS complex?

A
  • Less than or equal to 0.12 seconds
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39
Q

What should you think if the QRS complex is widened?

A

-BBB

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40
Q

Where would you see an R, R’ if there’s a RBBB?

A

-lead V1

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41
Q

Where should you see an R,R’ if there’s an LBBB?

A

-Lead V5

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42
Q

What would you think if there was an R, R’ in lead V1?

A

RBBB

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43
Q

What should you think if there’s an R,R’ in lead V5?

A

LBBB

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44
Q

What is the normal QTc (QT interval) for males?

A

<450

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45
Q

What is the normal QTc (QT interval) for females?

A

<460

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46
Q

What are the three mechanisms of tachyarrhythmias?

A
  • Enhanced automaticity
  • Reentry
  • Triggered Activity
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47
Q

What will be the response of a ventricular tachyarrhythmia to a vagal maneuver? Why?

A
  • little to no effect at all

- because there’s little to no parasympathetic innervation in ventricular cells

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48
Q

On what ion does nodal tissue primarily rely for initiating depolarization?

A

calcium

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49
Q

For a reentry to exist, what must be true about the Purkinge fiber with two conduction pathways to ventricular muscle?

A
  • there must be a limb with slow conduction

- each limb must have a different refractory period

50
Q

spontaneous depolarizations requiring a preceding impulse (a triggering beat)

A

after-depolarizations

51
Q

After-depolarization that occurs before membrane repolarization is complete

A

early after-depolarization

52
Q

Which after-depolarization may be the mechanism responsible for arrhythmogenesis related to the prolonged QT syndrome?

A

early after-depolarizations

53
Q

Which type of after-depolarization is often triggered by electrolyte disturbances?

A

early after-depolarizations

54
Q

After-depolarization that occurs after membrane repolarization is complete

A

delayed after-depolarization

55
Q

what can cause delayed after-depolarizations?

A

an abnormal intracellular calcium load high enough to cause spontaneous depolarization

56
Q

During what phase of repolarization do early after-depolarizations “strike”?

A

Phase 2 or 3

57
Q

During what phase of the myocardial action potential do delayed after-depolarizations arise?

A

Phase 4

58
Q

How can you calculate the upper rate range for sinus tachycardia?

A

220 - patient’s age

59
Q

What do we call it when patients have a rapid rise in HR with mild exertion?

A

-Inappropriate chronotropic response (part of inappropriate sinus tachycardia)

60
Q

What would the resting HR be of a patient with inappropriate sinus tachycardia?

A

> 100bpm

61
Q

What is the most common mechanism of PSVT?

A

-reentry involving AV node, atrium, or an accessory pathway

62
Q

Will junctional tachycardias terminate with vagal maneuvers?

A

no

63
Q

Accessory pathway between the atria and ventricles?

A

Bundle of Kent

64
Q

In what instances is WPW especially dangerous?

A

If patient has A fib or flutter

65
Q

DOC for WPW

A

IV procainamide

66
Q

What type of drug is best for treating WPW?

A

Na+ blocker

67
Q

What drug do we need to make sure patients with WPW syndrome don’t take?? Why?

A
  • Digoxin

- because it shortens the refractory period and may accelerate ventricular response in a setting of Afib

68
Q

Most common cardiac arrhythmia necessitating hospitalization in the US

A

Afib

69
Q

Which arrhythmia is associated with post-op status? On what post-op day does it most often occur?

A
  • Afib

- POD #3

70
Q

What signs of Afib might you witness as a result of the loss of atrial contractile force (and therefore decreased cardiac output)?

A
  • pulmonary rales
  • S3
  • peripheral edema (pitting)
  • JVD
71
Q

What is the focus of Afib treatment?

A
  • rate control
  • anticoagulation
  • restoration of sinus rhythm
72
Q

What drugs are good for the initial rate control of Afib an a hemodynamically stable patient?

A
  • IV diltiazem

- IV metoprolol

73
Q

What drug is commonly used for long-term anticoagulation?

A

Warfarin

74
Q

What INR do we want to achieve in our Afib patients before cardioverting?

A

2.0-3.0

75
Q

What is the most commonly used drug for Afib cardioversion?

A

IV Ibutilide

76
Q

How long must you maintain target INR before cardioverting Afib?

A

3-4 weeks

77
Q

Where is the reentry circuit that’s commonly associated with Aflutter located?

A

usually along the tricuspid valve annulus

78
Q

What kind of medical therapy is often implemented in a patient with Aflutter?

A
  • slow ventricular rate by drugs that increase AV block
  • restore sinus rhythm (slow conduction or prolong refractory period of the atria - Class IA, IC, or III)
  • DCCV if above fails
79
Q

Which ventricular arrhythmia is more common among young, healthy individuals?

A

PVCs

80
Q

What do we call it when there are more than three PVCs in a row?

A

ventricular tachycardia

81
Q

If a patient says they feel a “flip-flop” of their heart, what are they more than likely describing?

A

The onset of a normal beat after the compensatory pause that follows a PVC

82
Q

What is the most common cause of ventricular tachycardia?

A

CAD

83
Q

Why is it important to distinguish monomorphic VT from SVT with aberrant ventricular conduction?

A

They each require different immediate and long-term treatments

84
Q

When in doubt as to whether an arrhythmia is SVT with aberrant conduction or VT, which should you assume until proven otherwise?

A

VT

85
Q

prior structural heart disease - more likely VT or SVT?

A

VT

86
Q

vagal maneuvers affect the rhythm - SVT or VT?

A

SVT

87
Q

No relationship of the QRS to P wave - more likely SVT or VT?

A

VT

88
Q

QRS complexes in V1-V6 all have similar appearance - more likely SVT or VT?

A

VT

89
Q

When trying to determine if an arrhythmia is SVT with aberrant conduction or VT, in what circumstances is VT more likely?

A

-prior structural heart disease

90
Q

What is the most common cause of polymorphic VT?

A

-Acute MI

91
Q

What is the ultimate cause of Long QT Syndrome?

A
  • sodium and potassium chanelopathies

- this causes a prolongation of ventricular repolarizationd

92
Q

What’s the primary symptoms of Long QT Syndrome?

A

syncope

93
Q

What’s the hallmark arrhythmia of Long QT syndrome?

A

Torsades de Pointes

94
Q

What ion imbalances may be associated with Torsades?

A
  • hypokalemia

- hypomagnesemia

95
Q

What is the most common type of congenital Long QT syndrome?

A

LQT1

96
Q

What are common initiators of arrhythmias in LQT2 patients?

A
  • auditory stimuli

- emotional stress

97
Q

What factors can precipitate syncope and sudden death in LQT1 patients?

A
  • Physical exertion

- sympathetic stimulation

98
Q

What type of drug would you give to a patient with LQTS patient with a history of syncope or one with a definite prolonged QT interval?

A

Beta blocker

99
Q

What would you do with a LQTS patient already on a beta blocker who experiences recurrent syncope?

A

prophylactic implant of an ICD

100
Q

What diagnosis should you think of if a patient presents with a history of:

  • Unexplained syncope
  • Unexplained cardiac death of a family member <30
  • Congenital deafness
A

Long QT Syndrome

101
Q

What is the only effective therapy for ventricular fibrillation?

A

non-synchronized electrical defibrillation

102
Q

What are the two mechanisms of bradycardias?

A
  • disorders of impulse formation

- conduction blocks

103
Q

What are the most common extrinsic causes of sinus bradycardia?

A

medications

104
Q

What is the most common indication for a pacemaker?

A

Sick Sinus Syndrome

105
Q

What’s a good drug to give in a patient with severely depressed heart rate?

A

-IV atropine (anticholinergic)

106
Q

What type of pacing would you use in a patient when the AV node and vetnricular conduction systems function normally?

A

Atrial pacing (atria are paced)

107
Q

What type of pacing would you use in a patient with complete AV block?

A

P wave-triggered pacing (ventricles paced)

108
Q

What type of pacing would you use in a patient with SA node dysfunction combined with AV node dysfunction?

A

A-V sequential pacing (atria and ventricles are paced)

109
Q

If a junction escape rhythm did produce a P wave, in what leads would be inverted?

A

II, III, AVF (the inferior leads)

110
Q

What is the most common cause of 1’ AV block?

A

Drugs that slow conduction through the AV node (Beta blocker and calcium channel blockers)

111
Q

Which type of 2’ block is more serious?

A

Mobitz Type II

112
Q

Does a patient with a Wenckebach block need a pacemaker?

A

no

113
Q

Does a patient with a Mobitz block need a pacemaker?

A

Yes

114
Q

How are patients with Mobitz II block likely to present?

A

dizziness, lightneadedness, or syncope

115
Q

What is the most common cause of Mobitz II block?

A

Acute MI (anterior or inferior)

116
Q

Describe bradycardia management if perfusion is poor

A
  • Prepare for transcutaneous pacing
  • Administer IV Atropine
  • Begin pacing if Atropine ineffective
  • Consider epi or dopamine while waiting for pacer or if pacing is ineffective
117
Q

What are the two types of temporary pacing?

A
  • Transcutaneous

- Transvenous

118
Q

What should be included in your differential diagnosis for bradycardia?

A
  • SSS
  • Escape Rhythm
  • Afib/flutter
  • AV blocks
119
Q

What should be included in your differential diagnosis for tachycardia?

A
  • Sinus tach
  • SVT
  • Afib/flutter
  • MAT
  • Vtach
  • Vfib
120
Q

What should be included in your differential diagnosis for an irregular rhythm?

A
  • sinus arrhythmia if all P waves are the same
  • Wandering pacemaker if P waves are different
  • MAT if P waves are different
  • Atrial fibrillation if no P waves
  • Atrial flutter if there are flutter waves
  • AV blocks
121
Q

What should you think if you don’t see proper R wave progression?

A

-Something has happened to the anterior and/or lateral wall of the LV

Cardiology (8 decks)

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