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NURS 416 > Week 7a: Cardiac Arrhythmias > Flashcards

Week 7a: Cardiac Arrhythmias Flashcards

1
Q

P waves in sinus arrythmias

A

P waves are upright in I, II and aVF

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2
Q

Treatment for sinus bradycardia?

A

atropine 0.5mg q3-5min or adrenergic infusions such as dopamine or epinephrine IV

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3
Q

causes of sinus tachycardia

A

exercise, fever, and hyperthyroidism among others

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4
Q

treatment of sinus tachycardia

A

digoxin, beta blockers, CCBs, BBs, amiodarone

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5
Q

paroxysmal supra ventricular tachycardia

A

episodes of rapid heart rate that start in a part of the heart above the ventricles

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6
Q

what is the most common arrhythmia?

A

atrial fibrillation

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7
Q

chaotic and ineffective atrial depolarization

A

atrial fibrillation

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8
Q

signs and symptoms of atrial fibrillation

A

fainting, exercise intolerance, palpitations, pulmonary edema, decreased CO

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9
Q

medications for atrial fibrillation

A
  • anticoagulants
  • CCBs
  • BBs
  • cardiac glycosides
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10
Q

what is an intervention for atrial fibrillation?

A

atrial ablation

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11
Q

ECG of atrial fibrillation

A
  • tracing shows irregularly irregular rhythm with no P waves
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12
Q

which arrhythmia has the following characteristics?

  • regular ventricular rate of 150bpm
  • varying ratios of F waves to QRS complexes (most common is 4:1)
  • Sawtooth pattern
A

atrial flutter

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13
Q

which ECG will show a constant PR interval, greater than 2 seconds and all impulses conducted?

A

1st Degree AV block

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14
Q

Which arrhythmia results when each impulse is slower and slower and finally does not conduct an impulse, which results in a PR interval that gets longer and longer until a QRS complex is missing

A

2nd degree AV block type 1

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15
Q

Which arrhythmia has the following characteristics?

  • AV node conducts no impulses
  • atria and ventricles beat at an intrinsic rate (80 and 40 respectively)
  • no association between P waves and QRS complexes
A

3rd degree AV block

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16
Q

What are some characteristics of ventricular arrhythmias?

A
  • wide QRS complex
  • Variable rate
  • No P waves
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17
Q

what arrhythmia occurs earlier than the sinus beat, is wide and has no P wave?

A

Premature ventricular contraction

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18
Q

idioventricular rhythm

A
  • escape rhythm

- 20-40 bpm

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19
Q

which ventricular arrhythmia has a rate greater than 100 bpm

A

ventricular tachycardia

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20
Q

which type of ventricular tachycardia occurs secondary to prolonged QT interval?

A

Torsades des pointes

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21
Q

what type of ventricular arrhythmia includes unorganized activity of the ventricle?

A

ventricular tachycardia/fibrillation

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22
Q

which type of arrhythmia is life threatening, pulseless, with no CO?

A

Vfib and Vtach

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23
Q

vtach/vfib algorithm

A

1) CPR/IV/Access airway
2) Defibrillate 360 J
3) Epinephrine 1mg q3-5min
4) Amiodarone 300mg bolus

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24
Q

asystole algorithm

A

1) CPR/IV/Airway
2) Epinephrine 1mg q3-5min
3) consider pacing (low effectiveness)

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25
Q

class I drugs

A

act by blocking the fast sodium channels

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26
Q

class II agents

A

beta adrenergic blocking drugs that act by blunting the effect of sympathetic nervous system stimulation on the heart

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27
Q

class III agents

A

act by extending the action potential and refractoriness

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28
Q

class IV agents

A

act by blocking the slow calcium channels, thereby depressing phase 4 and lengthening phase 1 and 2

29
Q

procainamide is a?

A

sodium channel blocker

30
Q

therapeutic effects and uses for procainamide?

A

PAT, atrial flutter, atria fibrillation and prophylaxis of PSVT

31
Q

adverse effects of procainamide?

A

confusion and psychosis at high doses

32
Q

what is the primary indication of class IB drugs?

A

ventricular dysrhythmias

33
Q

class IB drugs work by?

A

shortening the refractory period

34
Q

Lidocaine is a?

A

Class IB drug

35
Q

class IC drugs….?

A

profoundly decrease conduction velocity

36
Q

what is the prototype drug of beta blockers?

A

propranolol

37
Q

beta blockers work by?

A

decreasing the conduction velocity

38
Q

what is the prototype drug of potassium channel blockers?

A

amiodarone

39
Q

therapeutic effects and uses of amiodarone?

A
  • atrial and ventricular dysrhythmias
  • resistant ventricular tachycardias
  • recurrent fibrillation
40
Q

what are some serious adverse effects of amiodarone?

A
  • pneumonia like syndrome

- prodysrhythmic action (arythmias)

41
Q

what is the prototype drug of calcium channel blockers?

A

verapamil

42
Q

which medication is contraindicated in ventricular dysthymias and must be carefully monitored for toxicity, drug interactions, and adverse effects

A

digoxin

43
Q

diastolic heart failure

A

signs and symptoms of heart failure with normal ejection fraction. mainly seen in elderly patients with hypertensive heart disease

44
Q

what results due to low cardiac output?

A

hypotension

45
Q

which condition includes peripheral edema, weight gain, liver congestion dysfunction and failure, renal hypertension, abdominal distension, LOC changes, and fatigue

A

right sided heart failure

46
Q

causes of right sided heart failure

A
  • conditions that restrict blood flow to the lungs
  • stenosis or regurgitation of the tricuspid or pulmonic valves
  • right ventricular infarction
  • cardiomyopathy
  • persistent life sided failure
  • acute or chronic pulmonary disease (for pulmonale)
47
Q

causes of left sided heart failure?

A
  • acute MI

- cardiomyopathy

48
Q

manifestations of left sided heart failure

A
  • SOB
  • crackles
  • pulmonary edema
  • exercise intolerance
  • cough and pink froth (rare)
49
Q

what is the result of fluid moving into the alveoli, causing lung stiffness, making lung expansion more difficult and impairs the gas exchange function of the lung

A

pulmonary edema

50
Q

How do ACEIs help in HF?

A
  • decrease vascular resistance
  • decrease secretion of aldosterone
  • decrease secretion of ADH
51
Q

what are some serious adverse effects of ACEIs?

A

Angioedema, cough, and hyperkalemia

52
Q

dobutamine and dopamine are examples of?

A

beta 1 adrenergic agonists

53
Q

what do beta1 adrenergic agonists do?

A

increase contractility of the heart to produce more powerful contractions but also reduce vasoconstriction and can produce dysrhythmias including tachycardia

54
Q

the effect of increased force of contraction of the heart when digoxin is a result of?

A

increased calcium in the cell

55
Q

what are some serious adverse effects of digoxin?

A

atrial dysrhythmias, sinus bradycardia, ventricular dysrhythmias, AV block

56
Q

what is often the first sign of digoxin toxicity?

A

nausea and vomiting

57
Q

what is the PO onset of digitalization?

A

30-120 mins

58
Q

What is the peak of PO digitalization?

A

2-6 hours

59
Q

how many days of digitalization until steady state is achieved?

A

7 days

60
Q

IV onset of digitalization?

A

5- 30 mins

61
Q

peak of IV digitalization

A

1-4 hours

62
Q

therapeutic level of digoxin?

A

0.8-2ng/ml

63
Q

toxic level of digoxin

A

> 2.4 ng/ml

64
Q

contraindications of digoxin

A
  • patients taking calcium channel blockers

- ventricular fibrillation

65
Q

Milrinone is a?

A

phosphodiesterase III inhibitor

66
Q

therapeutic effects and uses of milrinone (primacor)?

A

Short term treatment of life threatening heart failure

67
Q

mechanism of action of milrinone (primacor)

A

the persistence of cGMP results in vasodilation and a positive inotropic effect

68
Q

adverse effects of milrinone (primacor)

A

headache, nausea, vomiting, ventricular dysrhythmias

NURS 416 (17 decks)

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