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NUR 240 > NUR 240 ch 22 arrhythmias > Flashcards

NUR 240 ch 22 arrhythmias Flashcards

1
Q

arrhythmia definition

A

are disorders of the formation or conduction (or both) of the electrical impulse within the heart

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2
Q

arrhythmias are diagnosed by

A

analyzing the ECG waveform

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3
Q

sinus node (SA node)

A

the electrical impulse that stimulates and paces the cardiac muscle normally originates here. electrical impulse usually occurs at a rate of 60 to 100 times per minute

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4
Q

conduction

A

transmission of electrical impulse from one cell to another
ie. from the SA node to the AV node

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5
Q

depolarization

A

cardiac muscle cells change from a more negative charge to a more positive charge (still neg, but just a little less neg)

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6
Q

what happened during depolarization

A

contraction!! (systole)

influx of Na+ into the heart cell

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7
Q

repolarization

A

cardiac muscle cells return to a more negatively charged intracellular condition, their resting state

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8
Q

what happens during repolarization

A

REpolarization = RElaxation

(diastole)

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9
Q

P wave

A

part of an ECG that reflects conduction of an electrical impulse through the atrium

atrial depolarization

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10
Q

PR interval

A

the part of an ECG that reflects conduction of an electrical impulse from the sinoatrial node through the atrioventricular node

atrial depolarization complete

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11
Q

QRS complex

A

the part of an ECG that reflects conduction of an electrical impulse through the ventricles

ventricular depolarization

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12
Q

ST segment

A

the part of an ECG that reflects the end of the QRS complex to the beginning of the T wave

ventricular depolarization complete

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13
Q

QT interval

A

the part of an ECG that reflects the time from ventricular depolarization through repolarization

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14
Q

Sinus rhythm

A

electrical activity of the heart initiated by the sinoatrial node (SA)

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15
Q

U wave may be seen with a deficiency in which electrolyte

A

potassium

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16
Q

how can Potassium effect heart rhythm

A
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17
Q

heart rate is influenced by the

A

autonomic nervous system

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18
Q

Stimulation of the sympathetic nervous system causes

A
  • positive chronotropy (increased heart rate)
  • positive dromotrophy (increased AV conduction)
  • positive inotropy (increased force of myocardial contraction)
  • constricts peripheral blood vessels– increasing blood pressure
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19
Q

parasympathetic stimulation causes

A

negative chronotropy (reduces heart rate)
negative dromotropy (reduced AV conduction)
reduces force of atrial myocardial contraction
dilation of arteries– decreasing blood pressure

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20
Q

increased sympathetic stimulation can lead to

A

increased incidence of arrhythmias

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21
Q

causes of increased sympathetic stimulation

A

exercise, anxiety, fear, or administration of catecholamines such as dopamine, aminophylline, or dobutamine

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22
Q

causes of decreased sympathetic stimulation

A

with rest, anxiety reduction methods such as therapeutic communication or meditation, or administration of beta-adrenergic blocking agents

decreases incidence of arrhythmias

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23
Q

poor electrode adhesion can cause

A

significant artifact (distorted, irrelevant ECG waveforms)

wash skin with soap and water, do not wash sign with alcohol swab - hinders detection of cardiac electrical signal

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24
Q

skin prep for ECG electrodes

A

wash skin with soap and water
do not wash sign with alcohol swab - hinders detection of cardiac electrical signal

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25
Q

Arrhythmias can cause a disturbance of

A

both the rate and rhythm (or just one)

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26
Q

Atrial flutter

A

occurs because of a conduction defect in the atrium and causes rapid, REGULAR atrial impulse at a rate between 250 and 400 bpm

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27
Q

atrial fibrillation

A

results from abnormal impulse formation that occurs when structural or electrophysiologic abnormalities alter the atrial tissue causing rapid, disorganized, and uncoordinated twitching of the atrial musculature

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28
Q

causes of sinus bradycardia

A

lower metabolic needs (sleep, athletic training, hypothyroidism)
vagal stimulation (vomiting, suctioning, severe pain)
medications (calcium channel blockers [nifedipine, amiodarone], beta blockers [metroprolol])
idiopathic sinus node dysfunction
increased cranial pressure
CAD
MI
acute decompensated heart failure
acute altered mental status

29
Q

unstable and symptomatic bradycardia is frequently due to

A

hypoxemia (low blood oxygen)

30
Q

what med MAY be given if bradycardia produces signs and symptoms of clinical instability (acute AMS, chest discomfort, hypotension)

A

atropine

31
Q

sinus tachycardia causes

A

physiological or psychological stress (acute blood loss, shock, hypervolemia, hypovolemia, heart failure, pain, hyper metabolic states, fever, exercise, anxiety)
medications that stimulate sympathetic response (catecholamines, aminophylline, atropine), stimulants (caffeine and nicotine) and illicit drugs (amphetamines, cocaine, ecstasy)
autonomic dysfunction (Postural orthostatic tachycardia syndrome)

32
Q

Postural orthostatic tachycardia syndrome (POTS)

A

tachycardia without hypotension
presyncopal symptoms- palpitations, lightheadedness, weakness, and blurred vision that occurs with sudden postural changes

33
Q

As the heart rate increases, the diastolic filling time decreases, possibly resulting in reduced cardiac output and subsequent symptoms of syncope (fainting) and low blood pressure

If the rapid rate persists and the heart cannot compensate for the decreased ventricular filling, the patient may develop acute pulmonary edema

A
34
Q

medical management of tachycardia

A

Vagal maneuvers- such as carotid sinus massage, gagging, bearing down against a closed glottis (as if having a bowel movement)
forceful and sustained coughing
applying a cold stimulus to the face (such as applying an ice-cold wet towel to the face)
administration of adenosine

35
Q

if tachycardia is causing hemodynamic instability (acute AMS, chest discomfort, hypertension) what should be done?

A

synchronized cardioversion (if vagal maneuvers and adenosine are unsuccessful)

additionally:
IV beta blockers or calcium channel blockers

36
Q

cardioversion

A

electrical current given in synchrony with the patients own QRS complex to stop an arrhythmia

37
Q

atrial arrhythmias: premature atrial complexes (PAC)

A

a single ECG complex that occurs when an electrical impulse starts in the atrium before the next normal impulse of the sinus node

38
Q

what causes PAC

A

caffeine, alcohol, nicotine, stretched atrial myocardium (as in hypervolemia), anxiety, hypokalemia, hypermetabolic states (pregnancy), atrial ischemia, injury, infection, or infarction

39
Q

risk factors for a fib

A

INCREASING AGE**

COPD

*Hypertension

*Diabetes

*Obesity

*Valvular heart disease

*Heart failure

*Obstructive sleep apnea

*Alcohol abuse

*Hyperthyroidism

*Myocardial infarction

*Smoking

*Exercise

*Cardiothoracic surgery

*Increased pulse pressure

*European ancestry

*Family history

40
Q

common complication of a fib

A

blood pools in the atria which can lead to a stroke

41
Q

p waves in a fib

A

p waves are not present before the QRS complex
p waves are replaced with irregular fibrillary waves (F waves)

42
Q

atrial rate in a fib

A

very fast and irregular (300 to 600 bpm)

43
Q

uncontrolled a fib

A

ventricular rate is greater than 100 bpm, complications such as HF can develop

44
Q

patients with a fib should be on what medications

A

antithrombotic medications (anticoagulants and anti platelet drugs) because it reduces the risk of stroke

(to control HR) for persistent or permanent a fib- beta-blocker or non-dihydropyridine calcium channel blocker

45
Q

medications that can convert the heart rhythm or prevent atrial fibrillation

A

Medications that may be given to achieve pharmacologic cardioversion to sinus rhythm include flecainide, dofetilide, propafenone, amiodarone, and IV ibutilide

** dofetilide- monitor renal function and QT interval

46
Q

atrial flutter important feature

A

Because the atrial rate is faster than the AV node can conduct, not all atrial impulses are conducted into the ventricle, causing a therapeutic block at the AV node. This is an important feature of this arrhythmia. If all atrial impulses were conducted to the ventricle, the ventricular rate would also be 250 to 400 bpm, which would result in ventricular fibrillation, a life-threatening arrhythmia

47
Q

Atrial flutter signs and symptoms

A

chest pain, shortness of breath, low blood pressure

48
Q

medical management of atrial flutter

A

vagal maneuvers or administration of adenosine

49
Q

atrial fibrillation doesn’t allow for complete __

A

filling

50
Q

physical assessment of a patient with an arrhythmia

A

skin (pale and cool)
signs of fluid retention (JVD, lung auscultation)
rate and rhythm of apical and peripheral pulses
heart sounds
blood pressure, pulse pressure

51
Q

assess indicators of ___ and ____ in the assessment of patients with an arrhythmia

A

cardiac output

oxygenation

52
Q

pacemakers

A

electronic devices that provides electrical stimuli to heart muscle

set at a certain rate

53
Q

cardioversion vs defibrillation

A

cardioversion: delivery of electrical impulse is synchronized with patients ECG
defibrillation: delivery is unsynchronized

54
Q

If cardioverting, turn synchronizer ____
If defibrillating, turn synchronizer _____

A

on
off

55
Q

Ventricular arrhythmias: premature ventricular complex (PVC)

A

impulse that starts in the ventricle and is conducted through there ventricles before the next sinus impulse

can occur in healthy people with intake of caffeine, nicotine or alcohol

56
Q

PVCs are a common occurrence and may increase in frequency with age

A
57
Q

ventricular tachycardia (VT)

A

defined as three of more PVCs in a row, occurring at a rate exceeding 100 bpm

58
Q

Patients with larger MIs and lower ejection fractions are at higher risk of lethal VT.
VT is an emergency because the patient is nearly always unresponsive and pulseless.

A
59
Q

V tach looks like (on ECG)

A

tombstones

60
Q

treatment of choice for pulseless VT

A

defibrillation

61
Q

Torsades de pointes

A

a polymorphic VT preceded by a prolonged QT interval, which could be congenital or acquired

62
Q

what happens to cardiac output in V fib

A

decreases

63
Q

V fib is deadly if not reversed or treated

A
64
Q

ventricular fibrillation

A

the electrical conduction system is sending out an abnormal electrical signal that is causing the ventricles to quiver

ventricles quiver, not squeezing enough blood out

65
Q

what does V fib look like on a ECG

A

scribbles

chaotic, rapid rhythm that has no real organization to it

66
Q

V Fib: coarse fibrillatory waves

A

patient has a better chance at being revived

67
Q

V Fib: fine fibrillatory waves

A

slim chance for patient to be revived

looks similar to asystole on ECG

68
Q

Ventricular fibrillation is always characterized by the absence of an audible heartbeat, a palpable pulse, and respirations.

A
69
Q

medical management of V fib

A

early defibrillation is critical to survival with CPR

for refractory V fib- administration of amiodarone and epi may facilitate the return of a spontaneous pulse after defibrillation

NUR 240 (18 decks)

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