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NURS 425 > Exam #2: Dysrhythmias > Flashcards

Exam #2: Dysrhythmias Flashcards

1
Q

What are the properties of cardiac cells?

A
  • Automaticity
  • Excitability
  • Conductivity
  • Contractility
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2
Q

Automaticity

A

The ability to initiate an impulse spontaneously and continuously

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3
Q

Excitability

A

Is the ability of the heart to be stimulated

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4
Q

Conductivity of the Heart

A

the ability to transmit an impulse along a membrane in an orderly manner.

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5
Q

Contractility of the Heart

A

The ability to respond mechanically to an impulse

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6
Q

Review the conduction system of the heart

A

Watch on YouTube

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7
Q

ANS includes the

A
  1. Parasympathetic Nervous System

2. Sympathetic Nervous System

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8
Q

Parasympathetic Nervous System: Actions

A
  • Decreases rate of SA node
  • Slows impulse conduction of AV node

*Read notes

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9
Q

Sympathetic Nervous System: Actions

A
  • Increases rate of SA node
  • Increases impulse conduction of AV node
  • Increases cardiac contractility

*Read notes

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10
Q

Dysrhythmias

A

Disorder of impulse formation, conduction of impulses, or both

*add what’s left

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11
Q

ECG Monitoring

A
  • Graphic tracing of electrical impulses produced by heart

- Waveforms of ECG represent activity of charged ions across membranes of myocardial cells

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12
Q

Depolarization

A
  • The inside of the cell, when at rest, or in the polarized state, is negative compared with the outside.
  • When a cell or groups of cells are stimulated, the cell membrane changes its permeability.
  • *This allows sodium to move rapidly into the cell, making the inside of the cell positive compared with the outside
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13
Q

Repolarization

A

A slower movement of ions across the membrane restores the cell to the polarized state, called repolarization.

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14
Q

What does the P Wave represent?

A

represents time for the passage of the electrical impulse through the atrium causing atrial depolarization (contraction).

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15
Q

What does PR Interval represent?

A
  • Is measured from the beginning of the P wave to the beginning of the QRS complex.
  • It represents the time taken for the impulse to spread through the atria, AV node, and bundle of His; the bundle branches; and Purkinje fibers to a point immediately preceding ventricular contraction.
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16
Q

QRS Complex: Consist of three distinct waves, describe them.

A
  1. The Q wave is the first negative (downward) deflection after the P wave, short and narrow, and not present in several leads.
  2. The R wave is the first positive (upward) deflection in the QRS complex
  3. The S wave is the first negative (downward) deflection after the R wave.
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17
Q

Describe the ST Segment

A
  • is measured from the S wave of the QRS complex to the beginning of the T wave.
  • It represents the time between ventricular depolarization and repolarization (diastole).
  • It should be isoelectric (flat)
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18
Q

T Wave

A
  • The T wave represents the time for ventricular repolarization.
  • It should be upright.
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19
Q

QT Interval

A
  • The QT interval is measured from the beginning of the QRS complex to the end of the T wave.
  • It represents the time taken for entire electrical depolarization and repolarization of the ventricles.
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20
Q

What is the normal P Wave?

A

0.06-0.12

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21
Q

What is the normal PR Interval?

A

Normal PR Interval is 0.12-0.2

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22
Q

What is the normal QRS complex?

A

Normal QRS Complex is 0.04-0.12

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23
Q

What is a normal ST segment?

A

0.12

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24
Q

What is a normal T wave?

A

..

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25
Q

What is a normal QT interval?

A

0.4 to 0.44?

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26
Q

What does QRS complex represent?

A
  • The QRS interval is measured from the beginning to the end of the QRS complex.
  • It represents the time taken for depolarization (contraction) of both ventricles (systole).
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27
Q

12 lead ECG

A
  • Consists of 12 leads (or views) of the hearts activity.
  • May show changes suggesting structural changes, conduction disturbances, damage (ischemia or infarction), electrolyte imbalance or drug toxicity.
  • Helpful in assessment of Dysrhythmias.
  • Doesn’t care about lead placement
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28
Q

Calculating HR on ECG strip

A
  • Number of QRS complexes in 1 minutes (most accurate way to count)
  • R-R intervals in 6 seconds, and multiply by 10.
  • Number of small squares between one R-R interval, and divide this number into 1500
  • Number of large squares between one R-R interval, and divide this number into 300

*read notes and watch YouTube videos; practice!

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29
Q

Sinus bradycardia

A
  • The conduction pathway is the same as that in sinus rhythm but the SA node fires at a rate less than 60 beats/minute.
  • The rhythm is regular. The P wave precedes each QRS complex and has a normal shape and duration. The PR interval is normal, and the QRS complex has a normal shape and duration.
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30
Q

Sinus Bradycardia: Treatments include

A
  • Atropine
  • Pacemaker
  • Stop offending drugs
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31
Q

What are clinical manifestations of sinus bradycardia?

A
  • Hypotension
  • Pale, cool skin
  • Weakness
  • Angina
  • Dizziness or syncope
  • Confusion or disorientation
  • Shortness of breath
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32
Q

Sinus Tachycardia

A
  • The conduction pathway is the same in sinus tachycardia as that in normal sinus rhythm. The sinus rate is 101 to 200 beats/minute
  • The P wave is normal, precedes each QRS complex, and has a normal shape and duration. -The PR interval is normal, and the QRS complex has a normal shape and duration
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33
Q

Sinus Tachycardia Clinical Manifestations

A
  • Dizziness
  • Dyspnea
  • Hypotension
  • Angina in patients with CAD
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34
Q

Sinus Tachycardia: Treatments include

A
  • Guided by cause (i.e treat pain)
  • Vagal maneuver
  • B-blockers
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35
Q

Atrial Flutter

A

is an atrial tachydysrhythmia identified by recurring, regular, sawtooth-shaped flutter waves that originate from a single ectopic focus in the right atrium or, less commonly, the left atrium.

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36
Q

Atrial Flutter: The atrial rate is usually

A

200 to 350 beats/minute during a-flutter.

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37
Q

Atrial Flutter: Ventricular Rate

A

The ventricular rate will vary based on the conduction ratio.
In 2:1 conduction, the ventricular rate is typically found to be approximately 150 beats/minute.

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38
Q

Atrial Flutter: Atrial and Ventricular Rhythm/PR Interval and QRS complex

A
  • Atrial rhythm is regular, and ventricular rhythm is usually regular.
  • The PR interval is variable and not measurable.
  • The QRS complex is usually normal. Because the AV node can delay signals from the atria, there is usually some AV block in a fixed ratio of flutter waves to QRS complexes.
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39
Q

Atrial Flutter Treatment

A

-Pharmacologic agent:
A. Drugs used to control ventricular rate include CCB and Beta blockers
B: Antidysrhythmic Medications: convert atrial Flutter to sinus rhythm (ibutilide) or to maintain sinus rhythm (amiodarone, flecainide, drondarone)
-Electrical cardioversion (to convert a-flutter into a sinus rhythm in an emergency and electively)
-Radiofrequency ablation (treatment of choice for a-flutter)

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40
Q

Atrial Flutter Treatment: Primary Goal

A

slow the ventricular response by increasing AV block.

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41
Q

Atrial Fibrillation

A
  • Characterized by a total disorganization of atrial electrical activity due to multiple ectopic foci resulting in loss of effective atrial contraction.
  • At times, it may coexist with a-flutter
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42
Q

Atrial Fibrillation Characteristics (P waves, atrial rate, ventricular rate, PR interval, QRS complex

A
  • During atrial fibrillation, the atrial rate may be as high as 350 to 600 beats/minute.
  • P waves are replaced by chaotic, fibrillatory waves. (*ABSENT P WAVES!)
  • Ventricular rate varies and the rhythm is usually irregular.
  • The PR interval is not measurable, and the QRS complex usually has a normal shape and duration.
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43
Q

A-fib: When the ventricular rate is between 60 and 100 beats/minute,

A

it is atrial fibrillation with a controlled ventricular response

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44
Q

Atrial fibrillation with a ventricular rate greater than 100 beats/minute is

A

atrial fibrillation with a rapid (or uncontrolled) ventricular response.

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45
Q

A-fib and Stroke/CO

A

As with atrial flutter – causes a decrease in CO (d/t ineffective atrial contractions aka loss of atrial kick or a rapid ventricular response) and an increased risk of stroke (thrombi form in the atria d/t blood stasis)

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46
Q

A-fib: Treatment

A
  • Drugs to control ventricular rate (CCB, B-blockers, digoxin) and/or convert to sinus rhythm (amiodarone and ibutilide most common)
  • Electrical cardioversion
  • Anticoagulation
  • Radiofrequency ablation
  • Maze procedure with cryoablation

*Read notes for more information!

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47
Q

First Degree AV Block

A
  • Is a type of AV block in which every impulse is conducted to the ventricles but the time of AV conduction is prolonged.
  • After the impulse moves through the AV node, the ventricles usually respond normally.
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48
Q

Characteristics of First-Degree AV block (HR, P wave, PR interval and QRS complex)

A
  • HR is normal and rhythm is regular.
  • The P wave is normal
  • The PR interval is prolonged (greater than 0.20 second)
  • The QRS complex usually has a normal shape and duration.
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49
Q

Second Degree AV Block: Type I

A
  • Includes a gradual lengthening of the PR interval.
  • It occurs because of a prolonged AV conduction time until an atrial impulse is nonconducted and a QRS complex is blocked (missing).
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50
Q

Characteristics of AV Block Type I (Atrial rate, Ventricular rate, atrial/ventricular rhythm, P wave, QRS complex)

A
  • Atrial rate is regular, but ventricular rate may be slower because of nonconducted or blocked QRS complexes resulting in bradycardia.
  • Once a ventricular beat is blocked, the cycle repeats itself with progressive lengthening of the PR intervals until another QRS complex is blocked.
  • The rhythm appears on the ECG in a pattern of grouped beats.
  • Ventricular rhythm is irregular.
  • The P wave has a normal shape.
  • The QRS complex has a normal shape and duration.
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51
Q

Second Degree AV Block Type II

A
  • A P wave is nonconducted without progressive PR lengthening.
  • This usually occurs when a block in one of the bundle branches is present.
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52
Q

Characteristics of Second-Degree AV Block Type II (PR interval, atrial rate, Ventricular rate, P wave, QRS complex)

A
  • Atrial rate is usually normal. Ventricular rate depends on the degree of AV block.
  • Atrial rhythm is regular, but ventricular rhythm may be irregular.
  • The P wave has a normal shape.
  • The PR interval may be normal or prolonged in duration and remains constant on conducted beats.
  • The QRS complex is usually greater than 0.12 second because of bundle branch block.
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53
Q

Third Degree AV Heart Block

A

aka a complete heart block

  • Constitutes one form of AV dissociation in which no impulse from the atrial are conducted to the ventricles.
  • The atria are stimulated and contract independently of the ventricles.
  • The ventricular rhythm is an escape rhythm, and the ectopic pacemaker may be above or below the bifurcation of the bundle of His.
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54
Q

Characteristics of a Third-Degree AV Heart Block (Atrial rate, ventricular rate, atrial/Ventricular rhythms, P wave, PR interval and QRS complex)

A
  • The atrial rate is usually a sinus rate of 60 to 100 beats/minute.
  • The ventricular rate depends on the site of the block. If it is in the AV node, the rate is 40 to 60beats/minute, and if it is in the His-Purkinje system, it is 20 to 40beats/minute.
  • Atrial and ventricular rhythms are regular but unrelated to each other.
  • The P wave has a normal shape.
  • The PR interval is variable, and there is no relationship between the P wave and the QRS complex.
  • The QRS complex is normal if an escape rhythm is initiated at the bundle of His or above. It is widened if an escape rhythm is initiated below the bundle of His.
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55
Q

ECG Times: Small Squares

A

Represent 0.04 seconds.

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55
Q

ECG Times: Large Squares

A

Equal 0.20 seconds

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55
Q

ECG Voltage: Small Squares (1 mm) represent

A

0.1 mV

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55
Q

ECG Voltage: Large Squares equate to

A

0.5 mV

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55
Q

Preparing patient for ECG leads consist of

A
  • Clip excessive hair on chest wall
  • Rub skin with dry gauze
  • May need to use alcohol for oily skin
  • Apply electrode pad
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56
Q

Artifact

A
  • Distortion of the baseline and waveforms seen on the ECG.
  • Makes it difficult to interpret cardiac rhythm. May need to check the connections in the equipment or replace the electrodes if the conductive gel has dried out.
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57
Q

Telemetry Monitoring

A

Observing the HR and rhythm at a distant site.

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58
Q

What are two types of telemetry monitoring?

A
  • Centralized monitoring system (requires someone to continuously observe ECGs)
  • Advanced alarm system alerts when it detects dysrhythmias, ischemia or infarction.
59
Q

Steps to assessing a heart rhythm

A
  1. Look for the presence of the P wave. Is it upright or inverted? Is there one for every QRS complex or more than one? Are there atrial fibrillatory or flutter waves present?
  2. Evaluate the atrial rhythm. Is it regular or irregular?
  3. Calculate the atrial rate.
  4. Measure the duration of the PR interval. Is it normal duration or prolonged?
  5. Evaluate the ventricular rhythm. Is it regular or irregular?
  6. Calculate the ventricular rate.
  7. Measure the duration of the QRS complex. Is it normal duration or prolonged?
  8. Assess the ST segment. Is it isoelectric (flat), elevated, or depressed?
  9. Measure the duration of the QT interval. Is it normal duration or prolonged?
  10. Note the T wave. Is it upright or inverted?

Additional questions to consider include the following:

  1. What is the dominant or underlying rhythm and/or dysrhythmia?
  2. What is the clinical significance of your findings?
  3. What is the treatment for the particular rhythm?
60
Q

Normal Sinus Rhythm

A

-Normal sinus rhythm refers to a rhythm that starts in the SA node at a rate of 60 to 100 times per minute and follows the normal conduction pathway.
Rhythm is regular.
-The P wave precedes each QRS complex and has a normal shape and duration.
-The PR interval is normal, and the QRS complex has a normal shape and duration.

61
Q

What can cause sinus bradycardia?

A
  • Can occur in aerobically trained athletes and during sleep.
  • Can also occur in response to parasympathetic nerve stimulation and certain drugs (B-blockers, CCB)
  • Also associated with some disease states (i.e hypothyroidism, increase ICP, and inferior MI)
62
Q

What can cause sinus tachycardia?

A
  • Caused by vagal inhibition or sympathetic stimulation
  • Associated with physiologic and psychologic stressors (i.e pain, fever, hypovolemia, hypotension, anemia, hypoxia, hypoglycemia, MI, HF, hyperthyroidism, anxiety, etc.)
  • Drugs can increase rate (epinephrine, norepinephrine, atropine, caffeine, theophylline, hydralazine)
63
Q

What can cause atrial flutter?

A
  • Typically associated with disease
  • Symptoms result from high ventricular rate (>100/min) and loss of atrial “kick” (atrial contraction reflected by a sinus P wave) → decreased CO → heart failure
  • Increases risk of stroke (d/t increased risk of thrombus formation in the atria from the stasis of blood)
64
Q

What diseases/drugs can cause atrial flutter?

A
  • CAD
  • HTN
  • Mitral valve disorders
  • Pulmonary embolus
  • Chronic lung disease
  • Cor pulmonale
  • Cardiomyopathy
  • Hyperthyroidism
  • Drugs such as digoxin, quinidine and epinephrine
65
Q

What can cause atrial fibrillation?

A
  • Prevalence increases with age
  • Usually occurs in patients with underlying heart disease (CAD, HTN, cardiomyopathy, rheumatic heart disease,HF, pericarditis)
  • Can also occur with other disease states (thyrotoxicosis, alcohol intoxication, caffeine use, electrolyte disturbance, stress and heart surgery)
66
Q

What is the goal of treatment for atrial fibrillation?

A
  • Decrease ventricular response (to less than 100 beats/minute)
  • Prevent stroke
  • Convert to sinus rhythm, if possible
67
Q

Maze Procedure

A

a surgical intervention that stops atrial fibrillation by interrupting the ectopic foci that are responsible for the dysrhythmia. Incisions are made in both atria, and cryoablation (cold therapy) is used to stop the formation and conduction of these signals and restore normal sinus rhythm.

68
Q

What can cause first-degree AV block?

A

Associated with disease states and certain drugs:

  • MI
  • CAD
  • Rheumatic fever
  • Hyperthyroidism
  • Electrolyte imbalances (i.e hypokalemia)
  • Vagal stimulation
  • Drugs such as digoxin, beta-blockers, CCB
69
Q

Clinical Manifestations of First-Degree AV Block

A
  • Typically not serious

- Patients asymptomatic

70
Q

First-Degree AV Block Treatment

A
  • No treatment.

- Just monitor for any new changes in heart rhythm.

71
Q

What can cause a second-degree AV block Type I?

A
  • May result from drugs (i.e digoxin or beta-blockers) or CAD
  • Typically associated with ischemia (i.e myocardial ischemia or inferior MI)
  • Usually transient and well tolerated
72
Q

How do you treat second degree AV block Type I?

A
  • Atropine (to increase HR)
  • Pacemaker
  • If the patient is asymptomatic, monitor closely with a transcutaneous pacemaker on standby.
73
Q

What can cause second-degree AV block type II?

A
  • Associated with heart disease: Rheumatic heart disease, CAD, anterior MI and drug toxicity
  • Drug toxicity
74
Q

Second-Degree AV Block Type II can often be

A
  • Progressive (progresses to 3rd degree AV block).
  • Decreased HR results in decreased CO (subsequent hypotension and myocardial ischemia).
  • Poor prognosis
75
Q

How do you treat second-degree AV block type II?

A
  • Pacemaker if patient becomes symptomatic (hypotension, angina)
  • Atropine does NOT work for this dysrhythmia
76
Q

What can cause third-degree AV heart block?

A
  • Associated with severe heart disease: CAD, MI, myocarditis, cardiomyopathy
  • Some systemic diseases: amiloidosis and progressive systemic sclerosis
  • Certain drugs: digoxin, B-blockers and CCB
77
Q

Third-degree AV Heart Block Signs and Symptoms include

A
  • Decreased CO with subsequent ischemia, HF and shock.

- Syncope

78
Q

How do you treat a third-degree AV heart block?

A
  • Treat with pacemaker
  • Drugs to increase heart rate if needed while awaiting pacing (dopamine, epinephrine)
  • Atropine is NOT effective for this dysrhythmia
79
Q

Premature Ventricular Contractions

A
  • Is a contraction coming from an ectopic focus in the ventricles.
  • It is the premature or early occurrence of a QRS complex.
80
Q

Describe the shape of a premature ventricular contraction

A

-Wide and distorted QRS complex

81
Q

Mulitfocal PVC’s

A

PVCs that arise from different foci appear different in shape from each other

82
Q

Unifocal PVCs

A

PVCs that have the same shape

83
Q

Ventricular bigeminy

A

When every other beat is a PVC

84
Q

Ventricular Trigeminy

A

When every third beat is a PVC

85
Q

PVC Couplet

A

When there are two consecutive PVCs

86
Q

Ventricular Tachycardia occurs when there are

A

Three or more consecutive PVCs

87
Q

R-on-T phenomenon

A
  • occurs when a PVC falls on the T wave of a preceding beat.
  • This is especially dangerous because the PVC is firing during the relative refractory phase of ventricular repolarization.
  • Excitability of the heart cells increases during this time, and the risk for the PVC to start ventricular tachycardia or ventricular fibrillation is great.
88
Q

Characteristics of PVC’s (HR, Rhythm, P wave, PR interval, QRS complex, T wave)

A
  • HR varies according to intrinsic rate and number of PVCs
  • Rhythm is is irregular because of premature beats.
  • The P wave is rarely visible and is usually lost in the QRS complex of the PVC. Retrograde conduction may occur, and the P wave may be seen following the ectopic beat.
  • The PR interval is not measurable.
  • The QRS complex is wide and distorted in shape, lasting more than 0.12 second.
  • The T wave is generally large and opposite in direction to the major direction of the QRS complex.
89
Q

What can cause PVC’s?

A

Associated with:

  • Stimulants (i.e caffeine, alcohol, nicotine, digoxin)
  • Electrolyte imbalances, hypoxia, heart disease
  • Disease states associated with PVCs include MI, mitral valve prolapse, HF, cardiomyopathy and CAD.
90
Q

Clinical Manifestations of PVCs

A

Usually not harmful with normal heart but PVC’s may reduce CO and lead to angina and heart failure depending on frequency.

91
Q

Management of PVC’s

A
  • Because PVCs in CAD or acute MI indicate ventricular irritability, assess the patient’s physiologic response to PVCs.
  • Obtain the patient’s apical-radial pulse rate as PVCs often do not generate a sufficient ventricular contraction to result in a peripheral pulse. This can lead to a pulse deficit.
92
Q

PVC Treatment

A
  • Correct cause (i.e oxygen therapy for hypoxia, electrolyte replacement)
  • Antidysrhythmics (BB, procainamide, amiodarone)
93
Q

Ventricular Tachycardia

A
  • A run of three or more PVCs defines ventricular tachycardia (VT).
  • Ventricular rate is 150 to 250 beats/minute.
94
Q

Characteristics of Ventricular Tachycardia (Rhythm, P wave, QRS complex, T wave, the atria)

A
  • Rhythm may be regular or irregular
  • AV dissociation may be present, with P waves occurring independently of the QRS complex.
  • The atria may be depolarized by the ventricles in a retrograde fashion.
  • The P wave is usually buried in the QRS complex, and the PR interval is not measurable.
  • The QRS complex is distorted in appearance and wide (greater than 0.12 second in duration).
  • The T wave is in the opposite direction of the QRS complex
95
Q

Ventricular Tachycardia occurs when

A
  • Ventricular tachycardia occurs when an ectopic focus or foci fire repeatedly and the ventricle takes control as the pacemaker.
  • Different forms of VT exist, depending on QRS configuration. (Monomorphic and polymorphic; sustained and nonsustained)
96
Q

Why is ventricular tachycardia considered life-threatening?

A

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

97
Q

Ventricular Tachycardia is associated with

A
  • Heart disease (MI, CAD)
  • Significant electrolyte imbalances
  • Drug toxicity
  • CNS disorders
  • Can be seen in patients with no evidence of heart disease
98
Q

Ventricular Tachycardia can be stable versus non stable

A
  • Stable (patient has a pulse)

- Unstable (pulseless)

99
Q

Sustained Ventricular Tachycardia Clinical Manifestations

A

Causes severe decrease in cardiac output because of decreased ventricular diastolic filling times and loss of atrial contraction.This results in:

  • Hypotension
  • Pulmonary edema
  • Decreased cerebral blood flow
  • Cardiopulmonary arrest
100
Q

Ventricular Tachycardia Treatment

A
  • Precipitating causes must be identified and treated
  • VT with pulse: treated with antidysrhythmics or cardioversion
  • VT without pulse: treated with CPR and rapid defibrillation; followed by administration of vasopressors (epinephrine) and antidysrhythmics (amiodarone) If defibrillation was successful
101
Q

Ventricular Fibrillation

A
  • Is a severe derangement of the heart rhythm characterized on ECG by irregular waveforms of varying shapes and amplitude.
  • This represents the firing of multiple ectopic foci in the ventricle. Mechanically the ventricle is simply “quivering,” with no effective contraction, and consequently no CO occurs.
  • VF is a lethal dysrhythmia.
102
Q

Ventricular Fibrillation Characteristics (HR, Rhythm, P wave, PR interval and QR interval)

A
  • HR is not measurable
  • Rhythm is irregular and chaotic
  • The P wave is not visible
  • The PR interval and the QRS interval are not measurable.
103
Q

What can cause ventricular fibrillation?

A

Associated with:

  • MI
  • Ischemia
  • Disease states (HF and cardiomyopathy)
  • Procedures (cardiac pacing/catherization d/t catheter stimulation of the ventricle; thrombocytes therapyand coronary reperfusion)

Other clincial associations:

  • Hyperkalemia
  • Electric shock
  • Hypoxemia
  • Acidosis
  • Drug toxicity
104
Q

Ventricular Fibrillation Clinical Manifestations

A
  • Unresponsive, pulseless, and apneic

- If not treated rapidly, death will result

105
Q

How is ventricular fibrillation treated?

A
  • Treat with immediate CPR and ACLS
  • Defibrillation
  • Drug therapy (epinephrine and vasopressin)
106
Q

Asystole (May not need to know for test)

A

-Represents total absence of ventricular electrical activity
-No ventricular contraction

107
Q

Asystole Clinical Manifestations (may not need to know for test)

A
  • Patient is unresponsive, pulseless and apneic

- Must assess in more than one lead

108
Q

What causes asystole? (May not need to know for test)

A

Usually result of advanced cardiac disease, severe conduction disturbance, or end-stage HF

109
Q

Asystole Treatment (may not need to know for test)

A
  • Treat with immediate CPR and ACLS measures
  • Epinephrine and/or vasopressin
  • Intubation
  • Poor prognosis
110
Q

Pulseless Electrical Activity (may not need to know for test)

A
  • Electrical activity can be observed on the ECG, but no mechanical activity of the heart is evident, and the patient has no pulse
  • Prognosis is poor unless underlying cause quickly identified and treated
111
Q

PEA Treatment (may not need to know for test)

A
  • CPR followed by intubation and IV epinephrine

- Treatment is directed toward correction of the underlying cause

112
Q

Sudden Cardiac Death

A

Death from a cardiac cause

113
Q

Majority of SCDs result from:

A

ventricular dysrhythmias:

  1. Ventricular tachycardia
  2. Ventricular fibrillation
114
Q

Defibrillation is the treatment of choice for

A

VF and pulseless VT

115
Q

Defibrillation is most effective when

A

Most effective when completed within 2 minutes of dysrhythmia onset

116
Q

What is defibrillation?

A
  • Passage of DC electrical shock through the heart to depolarize myocardial cells
  • Allows SA node to resume pacemaker role
117
Q

Defibrillation output is measured in

A

Joules or watts per second

118
Q

What is the recommended energy for initial shocks in defibrillation?

A

Biphasic: 120 to 200 joules
Monophasic: 360 joules

119
Q

Defibrillation: After the first shock, what must be done immediately?

A

CPR

120
Q

Defibrillation Steps

A
  1. Start CPR while obtaining and setting up defibrillator
  2. Turn on and select energy
  3. Make sure sync button is turned off
  4. Apply gel pads
  5. Charge
  6. Position paddles firmly on chest
  7. Ensure “All clear”!!!!!
  8. Deliver charge
121
Q

Synchronized Cordioversion is the choice of therapy for

A

ventricular ( VT with a pulse) or supraventricular tachydysrhythmias

122
Q

What is synchronized cardioversion?

A

Synchronized circuit delivers a countershock on the R wave of the QRS complex of the ECG

123
Q

Synchronized Cardioversion Procedure

A
  • Procedure similar to defibrillation except sync button turned ON
  • If patient stable, sedate prior
  • Initial energy lower: 70–75 joules (biphasic) or 100 joules (monophasic)
  • If patient becomes pulseless, turn sync button off and defibrillate
124
Q

Implantable Cardioverter-Defibrillator (ICD) is appropriate for patients who

A
  • Have survived SCD
  • Have spontaneous sustained VT
  • Have syncope with inducible ventricular tachycardia/fibrillation during EPS
  • Are at high risk for future life-threatening dysrhythmias
125
Q

Benefit for the use of ICDs

A

Decreases mortality

126
Q

What is a implantable cardioverter-defibrillator and what does it do?

A
  • Consists of a lead system placed via subclavian vein to the endocardium
  • Battery-powered pulse generator is implanted subcutaneously
  • Sensing system monitors HR and rhythm – delivering 25 joules or less to heart when detects lethal dysrhythmia (VT or VF)
  • If the first shock is unsuccessful, the device recycles and continue to deliver shocks)
127
Q

ICD’s: Variety of emotions are possible including

A
  • Fear of body image change
  • Fear of recurrent dysrhythmias
  • Expectation of pain with ICD discharge
  • Anxiety about going home

*participation in an ICD support group should be encouraged

128
Q

What can you teach patients and caregivers about ICD’s?

A
  1. Follow-up appointments
  2. Incision care
  3. Arm restrictions
  4. Sexual activity
  5. Driving
  6. Avoid direct blows
  7. Avoid large magnets, MRI
  8. Air travel not restricted
  9. Avoid antitheft devices
  10. What to do if ICD fires
  11. Medic Alert ID
  12. ICD identification card
  13. Caregivers to learn CPR

*Read notes for more info if needed

129
Q

What are pacemakers?

A
  • Is an electronic device used to pace the heart when the normal conduction pathway is damaged
  • Paces the atrium and/or one or both ventricles
130
Q

Pacemakers: The pacing circuit consists of

A
  • Programmable pulse generator (power source)

- One or more conducting (pacing) leads to myocardium

131
Q

How do pacemakers work?

A
  • Pace atrium and/or one or both of ventricles
  • Most pace on demand, firing only when HR drops below preset rate: Sensing device inhibits pacemaker when HR adequate and pacing device triggers when no QRS complexes within set time frame
132
Q

Pacemakers: Antitachycardia pacing

A

Delivery of a stimulus to the ventricle to terminate tachydysrhythmias

133
Q

Pacemakers: Overdrive pacing

A

pacing the atrium at rates of 200–500 impulses/minute to terminate atrial tachycardias

134
Q

Permanent Pacemaker

A
  • A permanent pacemaker is implanted totally within the body.
  • The power source is placed subcutaneously, usually over the pectoral muscle on the patient’s nondominant side.
  • The pacing leads are placed transvenously to the right atrium and/or one or both ventricles and attached to the power source.
  • Pacing leads in both the atrium and the ventricle enable a dual-chamber pacemaker to sense and pace in both heart chambers.
135
Q

Permanent Pacemakers Indications

A

are inserted to treat patients with chronic heart problems in which the heart beats too slowly to adequately support the body’s circulation (i.e., AV heart blocks, sick sinus syndrome, atrial fibrillation with slow ventricular response, severe heart failure, cardiomyopathy, bundle branch block).

136
Q

Cardiac Resynchronization Therapy

A
  • Resynchronizes the heart cycle by pacing both ventricles
  • Biventricular pacing
  • Used to treat patients with heart failure
  • Can be combined with ICD for maximum therapy
137
Q

Temporary Pacemakers

A
  • Power source outside of the body.
  • They provide a bridge to insertion of a permanent pacemaker or until the underlying cause of the dysrhythmia is resolved.
138
Q

What are three types of temporary pacemakers?

A
  1. Transvenous
  2. Pericardial
  3. Transcutaneous
139
Q

Temporary Transvenous Pacemaker

A

consists of a lead or leads that are threaded transvenously to the right atrium and/or right ventricle and attached to the external power source

140
Q

Epicardial Pacing

A
  • Leads placed on epicardium during heart surgery

- Passed through chest wall and attached to external power source as needed

141
Q

Transcutaneous Pacing

A
  • For emergency pacing needs
  • Noninvasive
  • Bridge until transvenous pacer can be inserted
  • Use lowest current that will “capture”
  • Patient may need analgesia/sedation

*Read notes on slide

142
Q

Transcutaneous Pacing Placement (Not sure if need to know)

A
  • The TCP consists of a power source and a rate- and voltage-control device that attaches to two large, multifunction electrode pads.
  • Position one pad on the anterior part of the chest, usually on the V4 lead position, and the other pad on the back between the spine and the left scapula at the level of the heart.
  • The pads can be used for both pacing and defibrillation.
143
Q

Complications of Pacemakers

A
  • ECG monitoring for malfunction
  • Failure to sense (spontaneous atrial or ventricular activity): Causes inappropriate firing
  • Failure to capture (occurs when the electrical charge to the myocardium is insufficient to produce atrial or ventricular contraction): Lack of pacing when needed leads to bradycardia or asystole
144
Q

Pacemakers: Monitor for other complications including

A
  • Infection
  • Hematoma formation
  • Pneumothorax
  • Atrial or ventricular septum perforation
  • Lead misplacement

*Read notes on slide

145
Q

Pacemakers: Post procedure care

A
  • OOB once stable (out of bed)
  • Limit arm and shoulder activity (until incision heals)
  • Monitor insertion site for bleeding and infection
  • Patient teaching important

*Read notes on slide for more information

146
Q

Pacemaker: Patient and Caregiver Teaching

A
  • Follow-up appointments for pacemaker function checks
  • Incision care
  • Arm restrictions
  • Avoid direct blows
  • Avoid high-output generator
  • No MRIs unless pacer approved
  • Microwaves OK
  • Avoid antitheft devices
  • Travel not restricted
  • Monitor pulse
  • Pacemaker ID card
  • Medic Alert ID

*Read notes on slide for more information

147
Q

Radiofrequency Catheter Ablation Therapy

A
  • Electrode-tipped ablation catheter “burns” accessory pathways or ectopic sites in the atria, AV node, and ventricles
  • Postcare similar to cardiac catheterization
148
Q

Radiofrequency Catheter Ablation Therapy is the choice for

A

Nonpharmacologic treatment of choice for several atrial dysrhythmias

149
Q

Look at slides 92-99 and add info if not added after Tuesday’s lectures

A

…

NURS 425 (19 decks)

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