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NSG 410 MS II (mcp) > Unit 1: Dysrhythmias > Flashcards

Unit 1: Dysrhythmias Flashcards

1
Q

Bradydysrhythmias are defined as <__ bpm
Tachydysrhythmias are defined as >__ bpm

A

<60 bpm
>100 bpm

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2
Q

Premature complexes are _____ rhythm complexes that occur when a cardiac cell or cell group other than the SA node becomes irritable and fires an impulse before the next sinus impulse is produced.

A

Early rhythm complexes

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3
Q

Premature complexes, Bradydysrhythmias, and Tachydysrhythmias still have the impulse generated in the __ node but just have some other funky stuff going on.

A

SA node

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4
Q

Name some causes of Premature complexes

A
  1. Hypoxia
  2. Certain drugs/drug toxicity
  3. Caffeine
  4. Stress/Fear/Anxiety
  5. Electrolyte imbalances
  6. MI
  7. Hypovolemia (decreased blood volume)
  8. Nicotine
  9. Alcohol
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5
Q

Premature complexes may be _____, _____, _____, or occur repetitively in a _____ fashion.

A
  1. isolated
  2. irregular
  3. frequent
  4. rhythmic
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6
Q

Premature complexes may generate their impulse, aka an ectopic focus, by cells in _____, ______, or ________ tissue.

A
  1. atrial
  2. junctional
  3. ventricular tissue
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7
Q

______ exists when normal complexes and premature complexes occur alternatively in a repetitive two-beat pattern, with a pause occurring after each premature complex, so complexes occur in pairs.

A

Bigeminy

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8
Q

______ is a repeated three-beat pattern, usually occurring as two sequential normal complexes followed by a premature complex and a pause, with the same pattern repeating in triplets.

A

Trigeminy

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9
Q

______ is a repeated four-beat pattern, usually occurring as three sequential normal complexes followed by a premature complex and a pause, with the same pattern repeating itself in a four-beat pattern.

A

Quadrigeminy

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10
Q

Premature complexes are usually asymptomatic but can become symptomatic as they become more frequent.
What S/S might you see at that point?

A
  1. Palpitations
  2. Sxs of low cardiac output
  3. Irregular heartbeat

“Regularly Irregular”

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11
Q

A Premature ______ complex occurs when an impulse fires before the next SA node impulse is due. The EKG will show a complex with a premature (earlier) P-wave followed by a QRS complex with a shorter amplitude (height) between normal complexes.

A

Premature Atrial Complex (PAC)

Premature atrial contraction!
(Premature P-wave may not be visible if occurring so early that it’s embedded in the T-wave)

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12
Q

Teaching for pt’s with PACs

If PACs occur frequently, they may lead to more serious atrial ___________ which may require Tx.

A

Stress Mx, Avoid caffeine and ETOH

Atrial tachydysrhythmias

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13
Q

A Premature _______ complex on an EKG will show a complex with no P-wave and a premature QRS complex that’s rounded and wide, either elevated or depressed, uniform or multiform, between normal complexes.

A

Premature Ventricular Complex (PVC)

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14
Q

Uniform vs Multiform PVCs on an EKG

3 or more successive PVCs are called

A

Uniform (unifocal) → QRS complexes are the same shape
Multiform (multifocal) → QRS are different shapes

Non-sustained Ventricular Tachycardia (NSVTs)

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15
Q

PVCs are usually benign &/or Asymptomatic.
What assessment findings would present if the PVCs became symptomatic?

What can they be a warning sign of?

A
  1. Chest discomfort (increased stroke volume)
  2. Sxs of low perfusion (diminished or absent pulses, etc.)
  3. Poor oxygenation

An acute MI! → Life-threatening! Can trigger Vtach or Vfib!

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16
Q

What would you look at to determine the underlying cause of PVCs?

A
  1. Intake (caffeine, meds)
  2. Stress levels
  3. Electrolyte levels (hypokalemia or hypomagnesemia)
  4. CV assessment (pulses + apical, cap refill, color, temp,
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17
Q

How do we treat a non-perfusing PVC?

A

BBs

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18
Q

What are some benefits of Bradydysrhythmias?

A
  1. Decrease myocardial O2 demand
  2. Prolonged diastole → Improved perfusion to heart
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19
Q

What could a decreased BP + a Bradydysrhythmia result in?

A

Decreased perfusion to heart → Myocardial ischemia or infarction, dysrhythmias, hypotension, and HF

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20
Q

So, if you notice your patient has a Bradydysrhythmia, what should you immediately assess?

A

BP!
Then S/S of low perfusion: pulses, U/O, cap refill, skin color, mucous membranes etc.

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21
Q

What patient population would we be worried about if they had Tachydysrhythmia? Why?

A

Patients with CAD!

  1. Shorten diastole → Decrease heart perfusion
  2. Increase myocardial O2 demand
  3. Decreased Cardiac Output → Hypotension
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22
Q

Symptomatic Tachydysrhythmia may look like

A
  1. Palpitations
  2. Chest discomfort (pressure or pain from ischemia)
  3. Restlessness/Anxiety
  4. Pale, cool skin
  5. Hypotension → Syncope
  6. HF S/S (dyspnea, lung crackles, Distended neck veins, etc.)
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23
Q

Interventions for Symptomatic Tachydysrhythmias

A
  1. Oxygen
  2. Assess BP, pulses, perfusion, etc.
  3. Reduce Anxiety
  4. Identify the cause!
    - Infection/Sepsis? → Take a temp
    - Increased metabolic demands?
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24
Q

Dysrhythmias classified by their site of origin in the heart (3)

A
  1. Sinus dysrhythmia
  2. Atrial dysrhythmia
  3. Ventricular dysrhythmia
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25
Q

A _____ dysrhythmias have impulses that originate in the SA node and are caused by an imbalance in the SNS or PNS.

A

Sinus dysrhythmias

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26
Q

Sinus _________ is defined as a HR of 100-160 bpm, results from either SNS stimulation or PNS (vagal) inhibition, and has the same consequences as _____dysrhythmias.

A

Sinus Tachycardia;
Tachydysrhythmias
Shortened diastole → Decreased heart perfusion → Increased O2 demand → Increased work of heart → Decreased Cardiac Output → Hypotension

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27
Q

Increased SNS stimulation is a normal response to? (5)

A
  1. Physical activity
  2. Anxiety
  3. Pain
  4. Stress
  5. Drugs (Epi, Atropine, Caffeine, ETOH, Nicotine, cocaine)
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28
Q

Sinus tachycardia is also a compensatory response to decreased cardiac output or BP, as occurs in (6)

A
  1. Fever/Infection
  2. Anemia
  3. Hypoxemia
  4. Dehydration/FVD/Hypovolemic shock
  5. MI
  6. HF
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29
Q

Assessment for a patient with Sinus tachycardia

A
  1. Fatigue &/or Weakness; Restlessness &/or Anxiety
  2. Dyspnea &/or Orthopnea
  3. Hypoxia (Low SpO2)
  4. Pulse rate (increased)
  5. BP (decreased)
  6. Chest pain
  7. Palpitations
  8. U/O (decreased if impaired renal perfusion)
  9. ECG changes indicating MI
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30
Q

Desired treatment outcome for Sinus Tachycardia is to

A

Decrease HR by Identifying and treating the underlying cause

31
Q

Sinus _________ is defined as a HR of <60 bpm, results from either excessive PNS (vagal) stimulation or inhibition that causes a decreased rate of sinus node discharge, and can have the same benefits are ____dysrhythmias.

A

Sinus bradycardia ;
bradydysrhythmias
Prolonged diastole → Improved perfusion to heart →
Decreased O2 demand → Decreased work of heart

32
Q

Sinus bradycardias can result from (7)

A
  1. Vagal maneuvers (aka Valsalva maneuvers)
  2. vomiting
  3. suctioning
  4. Pain
  5. Hypoxia
  6. Drugs
33
Q

Name 3 drugs we use to induce sinus bradycardia

(think: heart meds)

A
  1. BBs
  2. CCBs
  3. Digoxin
34
Q

Who might naturally have a sinus bradycardia?

A

Athletes (strong heart muscles)

35
Q

Is Symptomatic sinus bradycardia a big deal?
What would it look like?

A

CODE SITUATION!

  1. Dizziness &/or weakness
  2. Syncope
  3. Confusion
  4. Hypotension
  5. Diaphoresis
  6. Dyspnea
  7. Chest pain
36
Q

Treatment of Symptomatic sinus bradycardia (4)

A
  1. Discontinue any causative drugs
  2. IV Atropine, 0.5 mg
  3. IV fluids
  4. Oxygen if SpO2 <94% or pt is SOB

extra info:
5. Admin Glucagon if cause is BB overdose (increases HR and BP)

37
Q

If the previous treatments don’t fix the sinus bradycardia and the patient is not perusing, ______ is indicated.

A

Pacing
Temporary Pacing or permanent pacemaker

38
Q

What are the two types of Temporary Pacing?
Indicate which is noninvasive or invasive.

A
  1. Temporary Transcutaneous Pacing → Noninvasive
  2. Temporary Transvenous Pacing → Invasive
39
Q

EXTRA INFO:
The two major modes of a pacing are _________ (demand) and _______ (fixed-rate) pacing.

A
  1. Synchronous → Demand pacing
  2. Asynchronous → Fixed-rate pacing
40
Q

_____ (location in hrt) pacing will result in a Pacer Spike before the p-wave on the EKG.

A

Atrial

41
Q

_____ (location in hrt) pacing will result in a Pacer Spike before the QRS complex on the EKG.

A

Ventricular

42
Q

_____ pacing will result in two Pacer Spikes, one before the p-wave and one before the QRS complex on the EKG. This type of pacing is used for ___ patients.

A

Biventricular pacing
HF patients

43
Q

Three types of Permanent pacemaker pacing

A
  1. Atrial (Sick Sinus)
  2. Ventricular
  3. Biventricular
44
Q

In _____ dysrhythmias, the focus of impulse generation shifts away from the SA node to the atrial tissues, resulting in a P-wave shape that differs from normal.

A

Atrial dysrhythmias

45
Q

3 types of Atrial dysrhythmias

A
  1. Premature atrial complexes
  2. Supraventricular tachycardia (SVT)
  3. Atrial fibrillation (Afib)
46
Q

Vagal maneuvers induce PNS (vagal) stimulation of cardiac conduction, specifically the SA and AV nodes.

What can they be used to treat? (1)
Name some examples (3)
Name any negative outcomes that can occur

A

Used to treat SVTs

  1. Carotid sinus massage (not really done anymore)
  2. Valsalva maneuver (hold breath+plug nose+bear down)
  3. Coughing/Gagging
  4. Diving reflex (hold breath + cold water on nostrils+face)

Negative consequences include rebound tachycardia, severe *bradycardia/bradydysrhythmias*, Vfib, asystole, and cerebral damage (p. 651)

47
Q

An EKG shows no P-wave and an irregular rhythm. What’s happening?

A

Atrial fibrillation (Afib)

48
Q

Name the disease states that are risk factors for developing Atrial fibrosis

A
  1. HTN
  2. CAD
  3. HF
49
Q

Interventions for Afib (6)

A
  1. Oxygen
  2. Reduce Anxiety
  3. Meds
  4. Synchronized Cardioversion
  5. Ablation
50
Q

When would we perform a cardioversion for a pt with Afib?

A

Unstable Afib = Afib + hypotension

51
Q

Medications for Afib (6)

(Indicate the DOC/most commonly used med)

A
  1. Diltiazem** (DOC, ACLS protocol)
  2. Amiodarone (2nd-line DOC)
  3. Dronedarone
  4. BBs (Atenolol, Metoprolol)
  5. Digoxin (HF-related)
  6. Anticoagulants (for sustained Afib)
52
Q

_________ __________ is caused by rapid stimulation of atrial tissue, has a normal rhythm, and a HR of 100-280 bpm.
When the rhythm is intermittent and initiated by a premature complex, such as a PAC, and terminated with or without intervention, it’s called _________ ______ ________.

A

Supraventricular tachycardia (SVT)

Paroxysmal Supraventricular tachycardia (PSVT)

53
Q

What would the EKG look like for Supraventricular tachycardia (SVT)?

A

Absent P-wave (it’s there, just embedded in the preceding T-wave)

54
Q

The S/S of SVT depends on the ______ of the SVT and the ____ of the ventricular response.

A

The S/S of SVT depends on the duration of the SVT and the rate of the ventricular response.

(S/S seen in *sustained* SVT)

55
Q

Treatment of Supraventricular tachycardia (SVT)

A
  1. Assess your patient!
    - Are they awake? BP?
  2. Identify the cause
  3. Vagal Maneuvers
  4. Adenosine (6mg, 12mg, 12mg) for acute episodes
  5. IV Fluids
  6. Meds for long-term Tx → BBs, CCBs
  7. Synchronized cardioversion (book says ablation p. 651)
56
Q

When do we perform a cardioversion for an SVT?

A

Unstable SVT = SVT + hypotension

57
Q

Name the 3 types of Ventricular Dysrhythmias

A
  1. Ventricular tachycardia (VTach)
  2. Ventricular Fibrillation (Vfib)
  3. Ventricular Asystole
58
Q

Are Ventricular Dysrhythmias a big deal?

A

OH YEAH! Can result in quick DEATH!

59
Q

Vagal maneuvers can be used to distinguish between _______ tachycardia and ________ tachycardia by slowing the rate of conduction at the SA or AV nodes

A

ventricular tachycardia and supraventricular tachycardia

If the vagal maneuver induces a decrease in HR → SVT

60
Q

Ventricular ______ occurs with repetitive firing of an irritable ventricle at a HR of 140-180 bpm or more, and may result from increased automaticity or re-entry mechanism.

A

Ventricular Tachycardia (VTach)

61
Q

VTach can be intermittent, aka ________ VTach, or _______ VTach that lasts >15-30 seconds.

A

Non-sustained VTach

Sustained VTach

62
Q

Risk Factors for VTach (5)

A
  1. myocardial ischemia
  2. cardiomyopathy
  3. Hypokalemia
  4. Drugs
  5. Shock
63
Q

Is VTach a big deal?

A

Doesn’t always result in cardiac arrest, but it is ALWAYS a problem!

64
Q

unstable VTach =

A

VTach + Hypotension

65
Q

Tx for stable VTach

A

GET THE DOCTOR!

  1. Cardioversion
  2. Antidysrhythmic Meds
66
Q

Tx of unstable VTach

A
  1. Cardioversion
  2. Antidysrhythmics (Amiodarone)
67
Q

Cardioversion used for (3)

A
  1. Unstable Afib
  2. Unstable SVT
  3. Unstable VTach
68
Q

Tx for Pulseless VTach

A

DEFIBRILLATE! “Unstable gets the cable!”

69
Q

Ventricular ________ is an EMERGENCY denoted by pulselessness and electrical chaos in the ventricles that can result in no ventricular contraction.

A

Ventricular Fibrillation (Vfib)

Ventricles Quiver and use loads of oxygen

Blood is not moving

Death is imminent unless we act!

70
Q

Risk factors for Vfib (5)

A
  1. CAD
  2. MI
  3. Hypokalemia or Hypomagnesemia
  4. Surgery, Procedure
  5. Trauma
71
Q

Tx for Vfib

A
  1. Start Compressions
  2. CALL CODE
  3. DEFIBRILLATE!

“Vfib = Defib!”

72
Q

Ventricular ______ occurs when know impulse is being conducted through the ventricles and is considered a terminal rhythm.

A

Ventricular asystole

No cardiac output

73
Q

Do we Defib for Ventricular asystole?

A

NO!

Treat underlying cause!

(Fluids, Bicarb, Electrolytes, Glucose)

74
Q

Tx for Ventricular asystole

A
  1. CPR
  2. Ventilate
  3. Epinephrine
  4. Treat underlying cause

NSG 410 MS II (mcp) (34 decks)

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