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Nursing 3: Test 3 > Dysrhythmias > Flashcards

Dysrhythmias Flashcards

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0
Q

Main Concern of Dysrhythmias

A
  1. Ineffective Tissue Perfusion
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1
Q

Dysrhythmias

A
  1. Any disturbance or irregularity in the electrical system of the heart
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4
Q

Electrophysiologic Properties

-Automaticity

A
  1. Ability of the pacemaker cells to initiate an electrical impulse
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5
Q

Electrophysiologic Properties

-Excitability

A
  1. Ability to respond to electrical impulse
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6
Q

Electrophysiologic Properties

-Conductivity

A
  1. Ability to transmit impulse from cell to cell
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7
Q

Electrophysiologic Properties

-Contractility

A
  1. Ability of muscle fibers to shorten in response to impulse
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8
Q

P Wave

A
  1. Atrial depolarization
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9
Q

QRS Wave

A
  1. Ventricle Depolarization

2. Atrial re-polarization

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10
Q

T Wave

A
  1. Ventricle Re-polarization
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11
Q

Refractory Periods

-Absolute Refractory Period

A
  1. Cell is unresponsive to another stimulus
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12
Q

Refractory Periods

-Relative Refractory Period

A
  1. A stimulus could initiate an action potential and cause a dysrhythmia
  2. Located at the last half of the T wave
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13
Q

QT Interval

A
  1. Ventricular Cycle
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14
Q

Normal PR Interval

A
  1. .12 to .20

- Time the impulse travels to AV node and bundle branches

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15
Q

Normal QRS Complex

A
  1. .06 to .10 seconds ( above .13 is considered above)
    - Ventricular depolarization
    - Q wave - first negative deflection
    - R Wave - first positive deflection
    - S Wave - First negative after R wave
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16
Q

ST Segment

-What to look for?

A
  1. If ST is Elevated, it indicates myocardial ischemia
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17
Q

Normal QT Interval

A
  1. 0.32 to 0.44

- Beginning of QRS to end of T wave

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18
Q

U Wave

A
  1. Usually NOT SEEN

2. May be seen with HYPOKALEMIA

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19
Q

Sick Sinus Syndrome

A
  1. Problems with impulse formation, transmission, & Conduction
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20
Q

Sinus Bradycardia

-Occurs in response to?

A
  1. Carotid sinus massage
  2. Hypothermia
  3. Increased vagal tone
  4. Parasympathomimetic drugs
  5. Hypothyroidism
  6. Obstructive jaundice
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21
Q

Sinus Bradycardia

-Clinical Significance

A
  1. Dependent on Symptoms
    - Hypotension
    - Pale, cool skin
    - Weakness
    - Angina
    - Dizziness or syncope
    - Confusion or disorientation // SOB
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22
Q

Sinus Bradycardia

-Treatment

A
  1. Atropine

2. Pacemaker may be required

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23
Q

Sinus Tachycardia

-Clinical Associations

A
  1. Associated w/ physiologic stressors
    - Exercise
    - Pain
    - Hypovolemia
    - MI, HF, Fever
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24
Q

Sinus Tachycardia

-Clinical Significance

A
  1. Dizziness & hypotension

2. Increased Myocardial oxygen consumption may lead to angina

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25
Q

Sinus Tachycardia

-Treatment

A
  1. Beta-adrenergic blockers to reduce HR and myocardial oxygen consumption
  2. Antipyretics to treat fever
  3. Analgesics for pain
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26
Q

Premature Atrial Contraction (PAC)

A
  1. Contraction originating from ECTOPIC focus in atrium (not in SA node)
  2. Travels across atrial by abnormal pathway
    - Creates distorted P wave
  3. May be stopped, delayed, or conducted normally at the AV node
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27
Q

Premature Atrial Contraction (PAC)

-Clinical Associations (Can result from)

A
  1. Emotional stress
  2. Use of caffeine, tobacco, alcohol
  3. Hypoxia
  4. Electrolyte imbalances
  5. COPD
  6. Valvular disease
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28
Q

Premature Atrial Contraction (PAC)

-Clinical Significance

A
  1. Isolated PAC’s are NOT SIGNIFICANT in those with healthy hearts
  2. In persons w/ heart disease, may be warning of more serious dysrhythmia
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29
Q

Premature Atrial Contraction (PAC)

-Treatment

A
  1. Depends on symptoms
    - Beta-Adrenergic blockers may be used to decrease PAC’s
    - Reduce or eliminate caffeine
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30
Q

Paroxysmal Supraventricular Tachycardia (PSVT)

A
  1. Originates in ectopic focus anywhere above bifurcation of bundle of HIS
  2. Some degree of AV block may be present
  3. Can occur in presence of Wolff-Parkinson-White syndrome
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31
Q

Paroxysmal Supraventricular Tachycardia (PSVT)

-Clinical Association In a Normal Heart

A
  1. Overexertion
  2. Emotional stress
  3. Stimulants
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32
Q

Paroxysmal Supraventricular Tachycardia (PSVT)

-Clinical Associations

A
  1. Digitalis toxicity
  2. Rheumatic heart disease
  3. CAD
  4. Cor pulmonale
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33
Q

Paroxysmal Supraventricular Tachycardia (PSVT)

-Clinical Significance

A
  1. Prolonged episode of HR > 180 BPM may precipitate decreased cardiac output
    - Palpitations
    - hypotension
    - Dyspnea
    - Angina
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34
Q

Paroxysmal Supraventricular Tachycardia (PSVT)

-Treatment

A
  1. Vagal maneuvers: Valsalva, coughing
  2. IV adenosine
  3. Cardioversion (make sure machine is set to synchronize)
  4. Ablation
    - Wolff-Parkinson-White (WPW)
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35
Q

Atrial Flutter

A
  1. Atrial Tachydysrhythmia identified by recurring, regular, SAWTOOTH-SHAPED flutter waves
  2. Originates from a single ectopic focus
  3. Loss of atrial kick
  4. Ration 4:1, 3:1, 2:1
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36
Q

Atrial Flutter

-Occurs with

A
  1. CAD, HTN
  2. Mitral valve disorders
  3. Pulmonary embolus
  4. Hyperthyroidism
  5. Digoxin, quinidine, epinephrine
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37
Q

Atrial Flutter

-Clinical Significance

A
  1. High Ventricular rates (>100) and loss of the atrial kick can decrease CO and precipitate HF, Angina
  2. Risk for Stroke due to risk of THROMBUS FORMATION in the atria
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38
Q

Atrial Flutter

-Treatment

A
  1. Drugs to slow HR: CCB, B-adrenergic blockers
  2. Electrical cardioversion
  3. Antidyshrythmia meds (amiodarone)
  4. Radiofrequency catheter ablation
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39
Q

Atrial Fibrillation

A
  1. Total disorganization of atrial electrical activity due to MULTIPLE ectopid foci
  2. Loss of effective atrial contraction and “kick”
  3. MOST COMMON dysrhythmia
  4. Prevalence increases w/ age
  5. “Irregularly Irregular”
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40
Q

Atrial Fibrillation

-How NCLEX describes it?

A
  1. “Irregularly Irregular”
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41
Q

Atrial Fibrillation

-Usually occurs with?

A
  1. Underlying heart disease, such as rheumatic heart disease, CAD
  2. Cardiomyopathy
  3. HF
  4. Pericarditis
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42
Q

Atrial Fibrillation

-Often acutely caused by?

A
  1. Thyrotoxicosis
  2. Alcohol intoxication
  3. Caffeine use
  4. Electrolyte disturbance
  5. Cardiac surgery
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43
Q

Atrial Fibrillation

-Clinical Significance

A
  1. Can result in decrease in CO
  2. Thrombi may form in the atria as a result of blood stasis
  3. Embolus may develop and travel to the brain, causing a stroke
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44
Q

Atrial Fibrillation

-Treatment for rate control?

A
  1. Digoxin
  2. B-adrenergic blockers
  3. CCB
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45
Q

Atrial Fibrillation

-Treatment (Long-term anticoagulation)

A
  1. Coumadin
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46
Q

Atrial Fibrillation

-Treatment used for Conversion

A
  1. Amiodarone
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47
Q

Atrial Fibrillation

-DC Cardioversion

A
  1. DC cardioversion may be used to convert atrial fibrillation to normal sinus rhythm
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48
Q

Atrial Fibrillation

-Rapid Ventricular Response

A
  1. This is very dangerous and needs to be put under control

2. Give pt Antidyshrythmia med

49
Q

Atrial Kick

A
  1. When the atria contract, it is responsible for pushing an extra 30% of blood into the ventricles
  2. The rest of the blood flows passively into the ventricles
50
Q

Electrophysiologic Properties

-All Properties

A
  1. Automaticity
  2. Excitability
  3. Conductivity
  4. Contractility
51
Q

Junctional Dysrhythmias

A
  1. Dysrhythmia that originates in area of AV node
  2. SA node has failed to fire or impulse has been blocked at the AV node
  3. Occasional retrograde conduction - inverted P wave
52
Q

Junctional Dysrhythmias

-Retrograde conduction

A
  1. Inverted P wave
53
Q

Junctional Dysrhythmias

-Clinical Associations

A
  1. CAD, HF
  2. Electrolyte imbalances
  3. Digoxin, amphetamines, caffeine, nicotine
54
Q

Junctional Dysrhythmias

-Clinical Significance

A
  1. Serves as safety mechanism when SA node has not been effective
  2. Escape rhythms should NOT be suppressed
  3. If rhythms are rapid, may result in reduction of CO and HF
55
Q

Junctional Dysrhythmias

-Treatment if symptomatic?

A
  1. Atropine if the Junctional dysrhythmia is slower than normal
  2. If it is faster (caused by digoxin) stop the underlying cause
56
Q

Junctional Dysrhythmias

-Treatment for Accelerated Junctional Rhythm

A
  1. If accelerated junctional rhythm and junctional tachycardia caused by digoxin toxicity…
  2. Digoxin is HELD
57
Q

Junctional Dysrhythmias

-Contraindicated treatment?

A
  1. Cardioversion is contraindicated
58
Q

Junctional Dysrhythmias

-Treatment if not caused by Digoxin Toxicity

A
  1. B-Adrenergic blockers
  2. CCB
  3. Amiodarone
    - Used for rate control for Junctional tachycardia
59
Q

Ventricular Dysrhythmias

A
  1. Affect CO and tissue perfusion
  2. Wide, bizarre QRS
  3. P wave w/ no relation to QRS, abnormal ST segment
  4. T wave w/ opposite deflection of QRS
60
Q

Premature Ventricular Contractions

A
  1. Contraction originating in ectopic focus of the ventricles
  2. Premature occurrence of wide and distorted QRS
  3. If it happens less than 3 times it is a PVC
  4. Always Say the Underlying rhythm **
61
Q

Premature Ventricular Contractions

-Clinical Associations

A
  1. Stimulants
  2. DIgoxin
  3. Electrolyte imbalance
  4. Hypoxia
  5. Fever
62
Q

Premature Ventricular Contractions

-Disease states that cause PVC’s?

A
  1. MI
  2. Mitral Valve prolapse
  3. HF
  4. CAD
63
Q

Premature Ventricular Contractions

-Clinical Significance w/ Normal Heart?

A
  1. Usually benign when heart is normal
64
Q

Premature Ventricular Contractions

-Clinical Significance with Diseased Heart?

A
  1. May decrease CO and precipitate angina and HF
    - Pt response to PVC’s must be monitored
    - PVC’s often do not generate sufficient ventricular contraction to result in peripheral pulse
    - Apical-radial pulse rate should be assessed to determine pulse deficit
65
Q

Premature Ventricular Contractions

-Clinical Significance

A
  1. Shows that there is some ventricular irritability
  2. May occur after:
    - Lysis of Coronary artery clot w/ Thrombolytic therapy in acute MI
    - Following plaque reduction after percutaneous coronary intervention
66
Q

Premature Ventricular Contractions

-Treatment

A
  1. Based on Cause of PVC’s
    - O2 therapy for hypoxia
    - Electrolyte replacement
    - Drugs:
    - –Beta-Adrenergic Blockers, Procainamide, Amiodarone, lidocaine
67
Q

Ventricular Tachycardia

A
  1. Run of Three or more PVC’s

2. Considered life-threatening because of decreased CO and the possibility of deterioration ventricular fibrillation

68
Q

Ventricular Tachycardia

-Classifications of V-Tach

A
  1. Monomorphic
  2. Polymorphic
  3. Sustained
  4. Non-sustained
69
Q

Ventricular Tachycardia

-Clinical Associations

A
  1. Electrolyte imbalances
  2. Long QT syndrome
  3. Digitalis toxicity
  4. MI & CAD
  5. CNS disorders
70
Q

Sustained Ventricular Tachycardia

-Clinical Significance

A
  1. Severe decrease in CO
    - Hypotension
    - Pulmonary edema
    - Decreased cerebral blood flow
    - Cardiopulmonary arrest
71
Q

Ventricular Tachycardia

-Clinical Significance

A
  1. VT can be stable (PT has pulse) or unstable (No pulse)
  2. Treatment for VT must be rapid
  3. May recur if prophylactic treatment is not initiated
  4. V-Fib may develop
72
Q

Ventricular Tachycardia

-Treatment

A
  1. Precipitating causes must be identified and treated (e.g hypoxia)
73
Q

Ventricular Tachycardia

-Treatment if Pt is hemodynamically stable (pulse + LV function)

A

Nursing Priority is to look for cause

  1. IV procainamide
  2. Sotalol
  3. Amiodarone or lidocaine
74
Q

Ventricular Tachycardia

-Treatment if Hemodynamically unstable

A
  1. Amiodarone or Lidocaine followed by CARDIOVERSION
75
Q

Ventricular Tachycardia

-Treatment if Patient Has NO PULSE? Unstable

A
  1. Initiate ACLS
  2. CPR and rapid defibrillation (Nursing Priority is to shock PT)**
    - Epinephrine (or Vasopressin) if defibrillation is unsuccessful
76
Q

Ventricular Fibrillation

-Top Causes

A
  1. Acute MI causes 50% of V-fib

In V-Fib you Defib for treatment

77
Q

Ventricular Fibrillation

A
  1. Severe derangement of the heart rhythm characterized on ECG by:
    - Irregular undulations of varying contour and amplitude
  2. No effective contraction of CO occurs
  3. Cardiac arrest
78
Q

Ventricular Fibrillation

-Clinical Associations

A
  1. VF may occur during cardiac pacing or cardiac cath
  2. VF may occur with coronary reperfusion after fibrinolytic therapy
  3. Electrical shock
  4. Hyperkalemia
  5. hypoxia / Acidosis / Drug toxicity
    * **Acute MI accounts for 50% of V Fib **TEST
79
Q

Ventricular Fibrillation

-Clinical Significance

A
  1. Unresponsive, pulseless, and apneic state
  2. If not treated rapidly, death will result
  3. MUST BE DEFIBRILLATED
80
Q

Ventricular Fibrillation

-Treatment

A
  1. Immediate initiation of CPR and ACLS
  2. Use of defibrillation and definitive drug therapy

Nursing Priority is to Defibrillate

81
Q

Asystole

A
  1. Represents total absence of ventricular electrical activity
82
Q

Asystole

-Clinical Associations

A
  1. Advanced cardiac disease
  2. Severe cardiac conduction system disturbance
  3. End-stage HF
83
Q

Asystole

-Clinical Significance

A
  1. Unresponsive, pulseless, and apneic state

2. Prognosis for asystole is extremely poor

84
Q

Asystole

-Treatment

A
  1. CPR w/ initiation of ACLS measures
    -Intubation
    -transcutaneous pacing
    -IV therapy w/ epinephrine and atropine
    NOT A SHOCKABLE RHYTHM (DO NOT DEFIBRILLATE)
85
Q

Pulseless Electrical Activity

A
  1. Electrical activity can be observed on the ECG, but there is no mechanical activity of the ventricles and the patient has no pulse
86
Q

Pulseless Electrical Activity

-Treatment

A
  1. CPR followed by intubation and IV epinephrine
  2. Atropine is used if the ventricular rate is slow
  3. Treatment is directed to correct underlying cause
87
Q

Sudden Cardiac Death

A
  1. Death occurring w/in 1 hour of onset of cardiovascular symptoms
  2. 1/2 die before reaching the hospital
  3. 25% to 30% survive
  4. 50% of cases are R/T CHD
88
Q

Sudden Cardiac Death

-Most Common Cause?

A
  1. Ventricular Fibrillation (80%)
89
Q

Sudden Cardiac Death

-Threat of Recurrence

A
  1. Threat of recurrence is greatest in the first 6-18 months following a major cardiac event

Educate the patient during this period to help them change habits

90
Q

Prodysrhythmia

-Clinical Significance

A
  1. Anti-dysrhythmic drugs may cause life-threatening dysrhythmias
91
Q

Prodysrhythmia’s

-Risk increases w/:

A
  1. Severe LV dysfunction

2. Digoxin and class IA, IC, and III antidysrhythmia drugs

92
Q

Prodysrhythmia’s

-Treatment

A
  1. First several days of drub therapy are the vulnerable period for developing Prodysrhythmias
  2. May oral antidysrhythmia drug regimens are initiated in a monitored hospital setting
93
Q

Electrophysiology Studies

A
  1. Analyze components of the heart’s electrical conduction system
    - Identifies sites of ectopic stimulation
  2. Ablative therapy
    - Destroys ectopic sites
94
Q

Fast Sodium Channel Blockers (Class I)

A
  1. Decrease flow of Na into cell
  2. Treat
    - PVC, VT, VF
95
Q

Beta-Blockers (Class II)

A
  1. Decrease automaticity, conduction, and contraction
  2. Treat:
    - SVT & prevent VF
96
Q

Potassium Channel Blockers (Class III)

A
  1. Decrease flow of K out of the cell
  2. Treat
    - VT, VF, SVT
97
Q

Calcium Channel Blockers (Class IV)

A
  1. Block flow of calcium into cell
98
Q

Defibrillation **

A
  1. Passage of electrical shock through the heart to depolarize the cells of the myocardium to allow the SA node to resume the role of pacemaker
99
Q

Defibrillation

-Used for what??

A
  1. Most effective method of terminating VF and pulseless VT
100
Q

Defibrillation

-How to use

A
  1. Use at any point in cardiac cycle
  2. VF and pulseless VT should be defibrillated immediately
  3. Remember “all clear” before shocking
101
Q

Synchronized Cardioversion

A
  1. Direct electrical current synchronized w/ the client’s rhythm
  2. Get consent
  3. Synchronize to the R wave
102
Q

Synchronized Cardioversion

-Uses

A
  1. SVT
  2. A Fib/Flutter
  3. Stable VT
103
Q

Synchronized Cardioversion

-Preparation

A
  1. Consent
  2. Emergency equipment
  3. IV, labs, VS, NPO
  4. Sedation as directed
104
Q

Synchronized Cardioversion

-Aftercare

A
  1. Reassessment of rhythm
  2. VS
  3. LOC
  4. Skin burns
105
Q

Implantable Cardioverter-Defibrillator (ICD)

-Appropriate for Patients who?

A
  1. Have spontaneous sustained VT
  2. Have syncope w/ inducible V-Tach/Fib during EPS
  3. Are at high risk for future life-threatening dysrhythmias
106
Q

Pacemaker Therapy

A
  1. Provides electrical stimulus to the heart when the heart fails to generate its own or the rate is too low
107
Q

Pacemaker Therapy

-Transcutaneous

A
  1. Pace through the chest wall
  2. SEDATE THE PATIENT TEST
  3. Machine is set to pacing
    One pad in the front of chest and one in the back
108
Q

Pacemaker Therapy

-Transvenous

A
  1. Electrode threaded into Right Ventricle or implanted during cardiac surgery
109
Q

Pacemaker Therapy

-Permanent

A
  1. Epicardial - sewn directly on the heart
  2. Endocardial -passed transvenously into the heart
  3. Subcutaneous pocket formed to hold generator
110
Q

Pacemakers

-Sensing

A
  1. Ability of the pacemaker to detect the heart’s own activity
111
Q

Pacemakers

-Pacing

A
  1. Atrial, Ventricular, Dual
  2. Rate
  3. Output
112
Q

Pacemakers

-Capture

A
  1. Successful stimulation

2. Seen on the EKG

113
Q

Catheter Ablation Therapy

A
  1. Electrode-tipped ablation catheter “burns” accessory pathways or ectopic sites in the atria, AV node, and ventricles
114
Q

Catheter Ablation Therapy

-Non-pharmacologic treatment for:

A
  1. AV nodal re-entrant tachycardia
  2. Re-entrant tachycardia r/t accessory bypass tracts
  3. Control of ventricular response of certain tachydysrhythmias
116
Q

Atrial fibrilation & Flutter

-At risk for?

A
  1. Thrombus **
117
Q

Pt Returning from Cath Lab

-What to look for?

A
  1. Hiccups show that there has been perforation of Right ventricle
118
Q

Torsades de Pointes

A
  1. Assess for long QT interval which can lead to torsades de pointes

Nursing 3: Test 3 (5 decks)

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