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Module 7 (Critical Care) > EKG > Flashcards

EKG Flashcards

1
Q

Adequate perfusion requires the heart to generate sufficient

A

cardiac output to distribute blood to the body tissues

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2
Q

Dysrhythmias can directly

A

decrease CO by changing stroke volume and heart rate

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3
Q

Tachycardia from a fever an decrease _____ and cause

A

CO; cause hypotension

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4
Q

Automaticity

A

ability to initiate an impulse spontaneously and continuously

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5
Q

Excitability

A

ability to be electrically stimulated

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6
Q

Conductivity

A

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

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7
Q

Contractibility

A

ability to respond mechanically to an impulse

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8
Q

What are the 4 properties of enabling the heart’s conduction system?

A

Automaticity
Excitability
Conductivity
Contractibility

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9
Q

Conduction System of the Heart purpose

A

sends signals to each part of the heart contracting and relaxing = control blood flow through your heart and to the rest of your body

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10
Q

What is the order of a normal cardiac impulse?

A
  • Sinoatrial (SA) node signals the atrial myocardium and causes the atrium to contract
  • Atrioventricular (AV) node
  • Bundle of His
  • Bundles Branches
  • Purkinje fibers impulses the ventricles
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11
Q

SA node is located in the

A

upper right atrium

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12
Q

Dysrhythmias result from disorders of what

A

impulse formation, conduction of impulses, or both

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13
Q

Which node is considered the pacemaker of the heart

A

SA node

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14
Q

SA node spontaneously fires how many times in a minute?

A

60-100 times a minute

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15
Q

What is the secondary pace maker

A

AV node automatically at its intrinsic rate

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16
Q

The AV node starts at a rate of

A

40-60 times per minute

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17
Q

The Bundle of His, Bundle Branches, and Purkinje fibers start at a rate of

A

20-40 times per minute

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18
Q

When the 2nd pacemaker starts firing more rapidly than the SA node, this causes?

A

Triggers early/late beats resulting in dysrhythmia replacing the normal sinus rhythm

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19
Q

Autonomic nervous system controls

A

Parasympathetic and sympathetic nervous systems
- rate of impulse formation
- speed of conduction
- strength of cardiac contraction

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20
Q

Parasympathetic Nervous System affects on the heart

A

decrease rate of SA node
slows impulse conduction of AV node
- pupils shrink
- slow, deep breaths, heart slows, gut active
Calm parachute

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21
Q

Sympathetic Nervous System affects on the heart

A

increase SA node
increase conduction of AV node
increase cardiac contractility
- pupils expand
- fast and shallow breaths
- heart pumps faster
- gut inactive

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22
Q

What components of the autonomic nervous system that affect the heart?

A

vagus nerve fibers of both parasym. / and sympathetic nervous systems

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23
Q

Stimulation of the vagus nerve causes

A

decrease rate of the SA node and slowed impulse conduction of the AV node

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24
Q

Stimulation of the sympathetic nerves increases what in conduction

A

increases SA node, AV impulse conduction and
cardiac contractility

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25
Q

Telemetry

A

observation of a patient’s HR and rhythm at a site distant from the patient.
- Centralized monitoring (Nurse and technician)
- Advanced Alarm Systems (Detect dysrhythmias, ischemia, or MI from a different location)

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26
Q

All telemetry patients should be assessed for

A

s/s of hemodynamic instability

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27
Q

Where do the 5 cardiac telemetry wires be placed?

A

Below right clavicle
- RA white
Below left clavicle
- LA black
Left lower rib cage
- LL red
Right lower rib cage
- RL green
Chest lead position
- MCL brown
not on bony prominences

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28
Q

The P wave represents*

A

SA node sending out an electrical impulse and represents atrial depolarization/contraction

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29
Q

QRS Complex represents

A

ventricular depolarization / contraction**.

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30
Q

In what way do the ventricles contract the heart?

A

endocardial to the epicardial (in - out)

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31
Q

What does it mean if the QRS Complex is wider than normal?

A

impulse started in the ventricles but there was a block delaying the impulse from completely contracting the heart

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32
Q

T and U waves represent

A

a resting spot for the heart to refill with blood

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33
Q

1 large square on an ECG is how long

A

0.20 seconds

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34
Q

How many large squares does it take to reach a full minute of ECG?

A

300

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35
Q

The time of an ECG is measured on what line

A

horizontal axis

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36
Q

The voltage of an ECG is measured on what line

A

vertical axis

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37
Q

Each small square is ____ mm and represents

A

1 mm = 0.04 seconds

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38
Q

10mm = ____ mVolt

A

1

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39
Q

The top lines on an ECG in bold mark what

A

3 seconds

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40
Q

How do you calculate HR on an ECG?

A

number of QRS coplexes in 1 minute
- QRS coplex in 6 seconds times 10 ~ HR in one minute

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41
Q

R wave is

A

first upward (positve) wave of the QRS complex

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42
Q

How do you determine regularity of a rhythm?

A

couning boxes btw waveforms (P wave to P wave or QRS to QRS

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43
Q

Marching out the rhythm =

A

determines early or late and hiding within another waveform

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44
Q

If the spaces between the waveforms are not equal =

A

irregular

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45
Q

How dod you determine if the pateint is hemodynamically stable?

A

BP
NH
RR
O2 Sat
cap refill

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46
Q

After determining the dysrhythmia is present, what is the priority?

A

determine the cause
- fever
- electrolyte

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47
Q

Treat the _______, not the monitor!

A

patient
- could be normal for them
- lead is off

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48
Q

What pulses are best to determine a pulse before starting CPR?

A

Carotid
Femoral

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49
Q

What should be assessed during a cardiac rhythm?

A

P wave (consistency, inverted)
P-R interval (prolonged)
Ventricular rate and rhythm (regular)
QRS complex (prolonged)
ST segment (flat, elevated. depressed)
Q-T interval
T wave (inverted)

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50
Q

Elongation of >0.2 PR interval means

A

slow conduction and heart block

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51
Q

What is artifact caused by?

A

leads and electrodes not secure
muscle activity (shivering)
electrical interference

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52
Q

Artifiact is

A

distortion of the baseline and waveforms seen on the ECG

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53
Q

What should the nurse do when she sees artifact?

A

check the patient not the rhythm
check connections in the equipment
replace electrodes
conductive gel
remove interference

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54
Q

Normal sinus rhythm rate

A

60-100 bpm

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55
Q

What starts normal sinus rhythm?

A

SA node and follows normal conduction pathways
- P wave - QRS complex (normal shape and duration

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56
Q

Sinus bradycardia

A

< 60 bpm with regular rhythm

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57
Q

Sinus bradycardia is normal for what type of people

A

aerobically trained athletes (runners)
people sleeping
Beta blockers
hypothyroidism
ask questions about why it could be so low

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58
Q

Sinus bradycardia can occur in response to

A

parasympathetic nervous system
carotid sinus massage
Valsalva manuever
hypothermia
increase intraocular pressure
vagal stimulation
Beta blockers, Calcium channel blockers

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59
Q

Common diseases associated with sinus bradycardia

A

hypothyroidism
increase intracranial pressure
hypoglycemia
inferior MI

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60
Q

S/S of Bradycardia

A

Hypotension
Pale, cool skin
Weakness
Angina
Dizziness or syncope
Confusion or disorientation
Shortness of breath

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61
Q

Tx for Bradycardia

A

Atropine
Pacemaker
Stop offending drugs (Hold, DC, or lower dose)

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62
Q

Symptomatic bradycardia is

A

a HR that is less than 60 beats/minute and is inadequate for the patient’s condition, causing the patient to experience symptoms

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63
Q

Atropine is what type of drug

A

anticholinergic (pt with symptoms)

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64
Q

Atropine for bradycardia (with symptoms) is

A

temporary fix and need to find a source

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65
Q

A patient’s cardiac rhythm is sinus bradycardia with a heart rate of 34 beats/minute. If the bradycardia is symptomatic, the nurse would expect the patient to exhibit
- Palpitations.
- Hypertension.
- Warm, flushed skin.
- Shortness of breath.

A
  • Shortness of breath.

Rational : Signs of symptomatic bradycardia include pale, cool skin, hypotension, weakness, dizziness or syncope, confusion or disorientation, and shortness of breath.

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66
Q

Sinus Tachycardia is

A

normal sinus rhythm 101-180 bpm

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67
Q

Sinus tachycardia is associated with what physiologic and psychologic stressors including

A

exercise
fever
pain
hypotension
hypovolemia
anemia
hypoxia
hypoglycemia
MI
HF
hyperthyoidism
anxiety
fear

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68
Q

What drugs can cause sinus tachycardia?

A

epinephrine (EpiPen), norepinephrine (Levophed), atropine (AtroPen),
caffeine,
theophylline (Theo-Dur), or hydralazine (Apresoline).
over-the-counter cold remedies have active ingredients (e.g., pseudoephedrine [Sudafed])

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69
Q

Will fluid bolus’ help tachycardia patients?

A

yes

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70
Q

Tachycardia s/s

A

depends on tolerance of the increased HR
Dizziness
Dyspnea
Hypotension - low CO
Angina in patients with CAD

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71
Q

Tx of Tachycardia

A

Guided by cause (e.g., treat pain)
Vagal maneuver – bearing down and take a deep breath, cough hard,
- NO ICE WATER ON THE FACE OR JUGULAR RUB as that is only for HCPs
β-adrenergic blockers (metoprolol)

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72
Q

PSVT means

A

Paroxymal Supravntricular Tachycardia

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73
Q

PSVT is caused by

A

ectopic focus anywhere above the bifurcation of the bundle of His. Identification of the ectopic focus is often difficult even with a 12-lead ECG as it requires recording the dysrhythmia as it starts

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74
Q

PSVT on EKG

A

absent P wave the faster it gets
- hidden in preceding T wave
- QRS interval is normal

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75
Q

PSVT bpm

A

151-220 (regular or slightly irregular)

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76
Q

PSVT occurs due to

A

reexcitation of the atria when there is a one-way block
- PAC

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77
Q

Paroxysmal refers to

A

abrupt onset and ending

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78
Q

Paroxymal SVT followed by

A

brief period of asystole

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79
Q

PSVT is associated with

A

overexertion
emotional stress
deep inspiration
caffeine and tobacco
rheumatic heart disease
dig toxicity
CAD
cor pulmonale

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80
Q

S/S of PSVT

A

HR is 150–220 beats/minute (add for clarification)
HR > 180 leads to decreased cardiac output and stroke volume
Hypotension
Dyspnea
Angina

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81
Q

PSVT with HR > 180 leads to

A

decreased CO and stroke volume

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82
Q

PSVT with HR > 180 s/s

A

Hypotension
Dyspnea
Angina

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83
Q

PSVT Tx

A

Vagal stimulation
IV adenosine (1st)
IV β-adrenergic blockers (sotalol)
Calcium channel blockers (diltiazeem and amiodarone)
Amiodarone
DC cardioversion

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84
Q

What are common vagal stimulation manuevers tx for PSVT?

A

Valsalva, coughing, and or (Singing, Humming, and Gargling)
-carotid massageonly a doctor should perform this one.

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85
Q

Adenosine’s half life is

A

short (10 seconds)

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86
Q

If vagal stimulation and drug therapy are ineffective for a PSVT and the patient becomes hemodynamically unstable, what should be used?

A

direct current cardioversion

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87
Q

Adenosine is what type of drug

A

antidysrhythmic

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88
Q

Adenosine for dx purpose can be used to

A

myocardial perfusion stress imaging study (vasodilator)

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89
Q

Adenosine for tx is used to

A

antidysrythmic for AVTs
- gives the heart a break for the SA node to take back control

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90
Q

When giving adenosine you should tell the patient about feeling

A

chest pressure after the medication is given
- injection in antecubital space close to the heart

91
Q

How should adenosine be given?

A

IV rapid (1-2 secs)
follow with 20mL flush rapid
stop cock setup

92
Q

What is the half-life of adenosine?

A

2-3 seconds

93
Q

If the patient given adenosine has asystole after delivery what should the nurse do?

A

continue to monitor as asystole is normal

94
Q

What equipment should a patient receiving adenosine have?

A

BP cuff
12 lead
cardiac monitor
defibrillator or AID ready

95
Q

What should you assess for on a patient receiving adenosine?

A

flushing, dizziness, chest pain, or palpitation

96
Q

What are the doses for adenosine?

A

6 mg
12 mg
Stop after the second, HCP can continue
- Cardioversion

97
Q

Atrial flutter is a

A

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

98
Q

Atrial flutter means

A

atria is not emptying

99
Q

Atrial flutter rates bpm

A

200-350

100
Q

The ventricular rate of atrial flutter will vary based on

A

conduction ratio
2:1

101
Q

The ventricular rate bpm in atrial flutter

A

150 bpm

102
Q

In atrial flutter, the atrial and ventricular rythms are regular/irregular.

A

regular

103
Q

Atrial flutter on EKG

A

P-R interval not measurable
QRS normal
**AV node delay signal to the atria - some AV block in fixed ratio

104
Q

If the atrial flutter is not hemodynamically stable then what s/s or hx is seen?

A

cardiac hx
medications
chest pain
SOB
sweat

105
Q

Atrial flutter is typically associated with

A

chronic lung disease, PE, cor pulmonale
cardiomyopathy
hyperthyoidism
HTN
CAD
mitral valve disorders

106
Q

What drugs can cause atrial flutter?

A

digoxin
quinidine
epinephrine

107
Q

Patients with atrial flutter have an increased risk of stroke because

A

risk of thrombus formation in the atria from the stasis of blood

108
Q

What is given to atrial flutter patients as a preventative of stroke

A

Warfarin

109
Q

Tx of Atrial Flutter

A

Pharmacologic agent – anti-dysrhythmic
Electrical cardioversion
Radiofrequency ablation

110
Q

The primary goal in treatment of atrial flutter is to

A

slow the ventricular response by increasing AV block

111
Q

What drugs are used to slow down ventricular response in atrial flutter

A

Calcium channel and beta blockers

112
Q

What is used to convert atrial flutter to sinus?

A

antidyrhythmic
- ibutilide [Corvert]
- amiodarone
- flecainide [Tambocor]
- dronedarone [Multaq]

113
Q

If the patient is hemodynamically unstable with atrial flutter or they elect to have it, what can be used

A

electrical cardioversion

114
Q

What is the treatment of choice for atrial flutter?

A

radiofrequency ablation
- catheter in the r. atrium
- low voltage and high frequency
- tissue is destroyed and normal sinus rhythm restored

115
Q

Atrial fibrillation causes the CO to

A

decrease = risk of stroke

116
Q

Atrial fibrillation results in

A

decrease in CO because of ineffective atrial contractions (loss of atrial kick) and/or a rapid ventricular response

117
Q

When the blood is stasis during a fib. =

A

clots form
- pass into the brain causing a stroke

118
Q

Paroxymal

A

spontaneous brief

119
Q

Persistent lasts for

A

7 days +

120
Q

A fib occurs in ___% of 65 + patients

A

6; increases with age

121
Q

A fib occurs in what diseases

A

underlying heart disease, such as CAD, rheumatic heart disease, cardiomyopathy, hypertensive heart disease, HF, and pericarditis

122
Q

Outside sources can cause a fib

A

acutely with thyrotoxicosis, alcohol intoxication, caffeine use, electrolyte disturbances, stress, and cardiac surgery

123
Q

A fib is charcterized as

A

total disorganization of atrial electrical activity due to multiple ectopic foci resulting in loss of effective atrial contraction

124
Q

Atrial rate during a fib

A

350-600 bpm

125
Q

P waves in a fib

A

chaotic, fibrillatory waves

126
Q

The ventricular rate of a fib is

A

irregular

127
Q

The ventricular rate of someone with a fib with controlled ventricular response?

A

60-100 bpm

128
Q

Atrial fibrillaion with rapid ventricular response rate is

A

> 100 bpm (uncontrolled)

129
Q

Tx for a fib.

A

slow the ventricular response by increasing AV block
Drugs to control ventricular rate and/or convert to sinus rhythm (amiodarone and ibutilide most common)
Electrical cardioversion (see about pain meds before)
Anticoagulation – Warfarin
Radiofrequency ablation – cath lab
Maze procedure with cryoablation

130
Q

The goal of a fib tx is to

A

decrease in ventricular repsonse <100 bpm
prevent stroke
conversion to sinus

131
Q

What drugs are used for ventricular rate control in a fib patients?

A

calcium channel blockers
beta blockers
digoxin
dronedarone

132
Q

What drugs are most common for chemical cardioversion?

A

amiodarone and ibutilide

133
Q

If a patient is in atrial fibrillation for longer than 48 hours, what is needed?

A

anticogulation therapy with warfarin for 3-4 weeks before cardioversion
- clots dislodge = stroke

134
Q

For patients with drug-refractory atrial fibrillation or who do not respond to electrical conversion what is used?

A

radiofrequency catheter ablation (similar to the procedure for atrial flutter) and the Maze procedure are further options.

135
Q

The Maze procedure is a surgical intervention that

A

stops atrial fibrillation by interrupting the ectopic electrical signals 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.

136
Q

If the pateint has a fib start with

A

electrical cardioversion then drugs

137
Q

If the patient has a SVT, start with

A

drugs then go to electrical cardioversion

138
Q

PVCs are known as

A

mide, bizarre, QRS

139
Q

PVC is a

A

contraction coming from an ectopic focus in the ventricles. It is the premature (early) occurrence of a QRS complex.

140
Q

Multifocal means

A

different in shape PVCs

141
Q

Unifocal PVC

A

PVCs remain the same

142
Q

Ventricular bigeminy

A

every other beat is PVC

143
Q

Ventricular trigeminy

A

every third beat is PVC

144
Q

Couplet PVC

A

two consecutive PVCs

145
Q

Ventricular tachycardia occurs when how many PVCS consecutive

A

3+

146
Q

R-on-T phenomenon occurs

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

147
Q

Excitability of the cardiac cells increase during

A

PVC - evolve into vent tachy or fibrillation

148
Q

PVC rhythm

A

irregular
- P wave rarely visible (lost in QRS)

149
Q

Retrograde conduction

A

P wave is inside the ectopic beat
- QRS distorted, prolonged, weird
- T - large and opposite direction of QRS

150
Q

If a hemodynamically stable patient has PVC, then

A

leave them alone

151
Q

What should you use to treat a patient having numerous PVCs

A

lidocaine

152
Q

PVCs are associated with

A

stimulants
electrolyte imbalances
hypoxia
fever
exercise
emotional stress
heart disease (MI, mitral valve prolapse, HF, and CAD)

153
Q

PVC patients need to be assessed for

A

apical-radial pulse deficit

154
Q

Tx for PVCs

A

Correct cause (O2 - hypoxia, replacement)
assess hemodynamic state
Antidysrhythmics - beta blockers, procainamide or amiodarone

155
Q

What are stimulants for PVCs?

A

caffeine, alcohol, nicotine, aminophylline, epinephrine, isoproterenol, and digoxin

156
Q

If a heart disease patient gets PVCs, then what will develop?

A

reduce the CO and lead to angina and HF depending on the frequency.
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, since PVCs often do not generate a sufficient ventricular contraction to result in a peripheral pulse. This can lead to a pulse deficit.

157
Q

Ventricular Tachycardia is

A

3+ PVCs (Tombstones)

158
Q

Ventricular rate of V Tach

A

150-250 bpm

159
Q

AV ____________ may be present, with P waves occurring independently of the QRS complex IN V.Tach

A

dissociation

160
Q

When V Tach is seen, what should you immediately do?

A

Start CPR when unconscious, if they are still alert it won’t last long so start large bore IV and calmly send you to cath lab

161
Q

Polymorphic V Tach =

A

Torsades de Pointes

162
Q

Torsades de Pointes means

A

twisting of the points

163
Q

Torsades de Pointes is a deficit of

A

magnesium

164
Q

With Torsades de Pointes, the nurse can give mag if

A

they know the mag level

165
Q

Tx for Torsades de Pointe

A

code, CPR AND, defibrillate them
Mag if know level

166
Q

Ventricular Tachycardia pacemaker

A

ectopic foci (ventricles take over)

167
Q

V Tach is considered life-threatening due to

A

decreased CO and the possibility of deterioration to ventricular fibrillation
- low perfusion = hypoxic = unconscious

168
Q

VT can quickly develop into

A

v fib

169
Q

V Tach is associated with

A

heart disease (MI, CAD, significant electrolyte imbalances, cardiomyopathy, mitral valve prolapse, long QT syndrome)
electrolyte imbalances
drugs toxicity
CNS disorder

170
Q

Sustained Vtach causes

A

decrease in CO because of decreased ventricular diastolic filling times and loss of atrial contraction

171
Q

Sustained V tach results in

A

hypotension, pulmonary edema, decreased cerebral blood flow, and cardiopulmonary arrest

172
Q

Unstable V tach

A

pulseless

173
Q

Stable V Tach

A

pulse

174
Q

Stable V tach tx

A

VT with pulse (stable) treated with antidysrhythmics or cardioversion
- IV procainamide, sotalol, or amiodarone

175
Q

Unstable V tach Tx

A

CPR and rapid defibrillation
vasopressors (epinephrine) antidyrhthymic (amiodarone)

176
Q

If the VT is polymorphic with a normal baseline Q-T interval, any one of the following drugs is used:

A

β-adrenergic blockers, amiodarone, procainamide, or sotalol.

177
Q

Polymorphic VT with a prolonged baseline Q-T interval is treated with

A

IV magnesium, isoproterenol, phenytoin (Dilantin), or antitachycardia pacing

178
Q

dofetilide does what to QT interval

A

prolongs

179
Q

V fib is a

A

severe derangement of the heart rhythm characterized on ECG by irregular waveforms of varying shapes and amplitude

180
Q

V fib is firings of

A

multiple ectopic foci in the ventricle. Mechanically the ventricle is simply “quivering,” with no effective contraction, and consequently no CO occurs
chaotic squiggles

181
Q

In v fib, what is the heart rate

A

not measurable

182
Q

V fib is associated with

A

MI, ischemia, disease states in the heart (HF and cardiomyopathy), procedures (cardiac pacing and catheterization)
- coronary reperfusion after thrombolytic therapy
- electric shock, hypoxemia, acidosis, drug toxicity

183
Q

V fib patients are usually

A

unresponsive, pulseless, and apneic state.

184
Q

Tx for v fib

A

with immediate CPR and ACLS
Defibrillation ACLS
Drug therapy (epinephrine, vasopressin)**

185
Q

A patient in the coronary care unit develops ventricular fibrillation. The first action the nurse should take is to

Perform defibrillation.
Initiate cardiopulmonary resuscitation.
Prepare for synchronized cardioversion.
Administer IV antidysrhythmic drugs per protocol.

A

Initiate cardiopulmonary resuscitation.

Rationale: Immediate treatment for ventricular fibrillation is the initiation of Cardiopulmonary resuscitation, followed by the use of defibrillation and definitive drug therapy according to advanced cardiac life support guidelines.

186
Q

Asystole represents

A

total absence of ventricular electrical activity
- no depolarization = no contractions

187
Q

Asystole patients are found

A

unresponsive, pulseless, and apneic

188
Q

With asystole patients check the rhythms in

A

all leads

189
Q

Tx of Asystole

A

Treat with immediate CPR and ACLS measures
- do not defibrillate
Epinephrine and/or vasopressin
Intubation
Poor prognosis
- take a pulse, cap refill, O2, BP, lead check, start CPR

190
Q

Asystole result in

A

advanced cardiac disease, severe conduction disturbance, or end-stage HF
- prolonged arrest usually not able to be resuscitated

191
Q

PEA

A

Electrical activity can be observed on the ECG, but no mechanical activity of the ventricles is evident, and the patient has no pulse

192
Q

PEA has no

A

mechanical movement of the heart
- poor prognosis unless cause is tx

193
Q

The most common causes of PEA
Hs and Ts

A

Hypovolemia,
hypoxia,
Hydrogen ion (metabolic acidosis)
hyper/hypokalemia,
hypoglycemia,
hypothermia

Toxins (e.g., drug overdose),
cardiac tamponade,
thrombosis (e.g., MI, pulmonary embolus),
tension pneumothorax
trauma.

194
Q

Treatment for PEA

A

CPR followed by intubation and IV epinephrine
Treatment is directed toward correction of the underlying cause
DO NOT SHOCK to not knock the electrical system
ALWAYS touch the patient to confirm

195
Q

Third-Degree AV Heart Block

A

complete heart block, constitutes one form of AV dissociation in which no impulses from the atria are conducted to the ventricles

196
Q

Third-Degree AV Heart Block is caused by what in the heart

A

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.
Cardiac output is depleting and the P waves do not fit together

197
Q

Third-Degree AV Heart Block
- atrial rate AV

A

40-60 bpm

198
Q

Third-Degree AV Heart Block
- Purkinje fibers rate

A

20-40 bpm

199
Q

Third-Degree AV Heart Block is associated with

A

severe heart disease (CAD, MI, myocarditis, cardiomyopathy, some systemic diseases (amyloidosis, scleroderma, certain drugs (digoxin, β-adrenergic blockers, and calcium channel blockers)

200
Q

Third-Degree AV Heart Block usually results in

A

decreased CO

201
Q

Third-Degree AV Heart Block leads to

A

syncope, HF, shock
- severe bradycardia to periods of asystole

202
Q

Third-Degree AV Heart Block Tx

A

symptomatic - permanent trancutaneous pacemaker ASAP

203
Q

Temporary Tx for Third-Degree AV Heart Block

A

atropine, dopamine (Intropin), and epinephrine is a temporary measure to increase HR and support blood pressure until temporary pacing is started. Patients will need a permanent pacemaker as soon as possible.

204
Q

Isoelectric line is

A

flat and represents those normal times in the cardiac cycle when the ECG is not recording any electrical activity in the heart

205
Q

St-segment elevation associated with

A

myocardial injury (STEMI)
- Q wave is prolonged
- R is elevated and prolonged
- tx cath lab within 90 minutes

206
Q

ST segment depression and T inversion is in a

A

NSTEMI
- tx medically

207
Q

Biphasmic Defibrillation joules

A

120-200 J

208
Q

Monophasmic Defibrillation joules

A

360 J

209
Q

After the first shock of defibrillation,

A

start CPR immediately beginning with chest compressions.

  • give it time to go back to rhythm
210
Q

Cardioversion needs to

A

sync with Q waves for shock

211
Q

Cardiac Pacemaker

A

electronic device used to pace the heart when the normal conduction pathway is damaged
- control heart rate with compromised conduction

212
Q

Single chamber pacemaker

A

either atria or ventricles

213
Q

Dual chmaber pacemaker

A

paces both atrium and ventricles

214
Q

Capture measn

A

electrical charge produces atrial or ventricular contraction

215
Q

Sensed

A

recognize spontaneous atrial or ventricular activity

216
Q

Permanent Pacemaker is

A

implanted

217
Q

Temporary Pacemaker

A

power source outside the body
- transvenous, epicrdial, trancutaneous

218
Q

Trancutaneous Pacemakers

A

noninvasive, temporary procedure used until a transvenous pacemaker is inserted or until more definitive therapy is available

219
Q

Where do you place the pads for defibrillation?

A

R upper part of chest and L lower part of chest with the heart in the middle to transfer energy

If anterior and posterior pads are available do those

220
Q

Failure to senseoccurs

A

pacemaker fails to recognize spontaneous atrial or ventricular activity, and it fires inappropriately. This can result in the pacemaker firing during the excitable period of the cardiac cycle, resulting in VT. Failure to sense is caused by fibrosis around the tip of the pacing lead, battery failure, sensing set too high, or dislodgment of the electrode.

221
Q

Failure to capture

A

when the electrical charge to the myocardium is insufficient to produce atrial or ventricular contraction. This can result in serious bradycardia or asystole. Failure to capture is caused by pacer lead damage, battery failure, dislodgment of the electrode, electrical charge set too low, or fibrosis at the electrode tip.

222
Q

What are the lethal dysrhythmias?

A

Vtach
Vfib
Asystole
3 degree Heart Block

223
Q

What are shockable rhythms?

A

V tach and v Fib

224
Q

Rhythms that can cardiovert

A

SVT
Afib
Aflutter

Module 7 (Critical Care) (22 decks)

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