Module 7 (Critical Care) > EKG > Flashcards

EKG Flashcards

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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
Telemetry
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)
26
All telemetry patients should be assessed for
s/s of hemodynamic instability
27
Where do the 5 cardiac telemetry wires be placed?
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*
28
The P wave represents*
SA node sending out an electrical impulse and represents atrial depolarization/contraction
29
QRS Complex represents
ventricular depolarization / contraction**.
30
In what way do the ventricles contract the heart?
endocardial to the epicardial (in - out)
31
What does it mean if the QRS Complex is wider than normal?
impulse started in the ventricles but there was a block delaying the impulse from completely contracting the heart
32
T and U waves represent
a resting spot for the heart to refill with blood
33
1 large square on an ECG is how long
0.20 seconds
34
How many large squares does it take to reach a full minute of ECG?
300
35
The time of an ECG is measured on what line
horizontal axis
36
The voltage of an ECG is measured on what line
vertical axis
37
Each small square is ____ mm and represents
1 mm = 0.04 seconds
38
10mm = ____ mVolt
1
39
The top lines on an ECG in bold mark what
3 seconds
40
How do you calculate HR on an ECG?
number of QRS coplexes in 1 minute - QRS coplex in 6 seconds times 10 ~ HR in one minute
41
R wave is
first upward (positve) wave of the QRS complex
42
How do you determine regularity of a rhythm?
couning boxes btw waveforms (P wave to P wave or QRS to QRS
43
Marching out the rhythm =
determines early or late and hiding within another waveform
44
If the spaces between the waveforms are not equal =
irregular
45
How dod you determine if the pateint is hemodynamically stable?
BP NH RR O2 Sat cap refill
46
After determining the dysrhythmia is present, what is the priority?
determine the cause - fever - electrolyte
47
Treat the _______, not the monitor!
patient - could be normal for them - lead is off
48
What pulses are best to determine a pulse before starting CPR?
Carotid Femoral
49
What should be assessed during a cardiac rhythm?
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)
50
Elongation of >0.2 PR interval means
slow conduction and heart block
51
What is artifact caused by?
leads and electrodes not secure muscle activity (shivering) electrical interference
52
Artifiact is
distortion of the baseline and waveforms seen on the ECG
53
What should the nurse do when she sees artifact?
**check the patient not the rhythm** check connections in the equipment replace electrodes conductive gel remove interference
54
Normal sinus rhythm rate
60-100 bpm
55
What starts normal sinus rhythm?
SA node and follows normal conduction pathways - P wave - QRS complex (normal shape and duration
56
Sinus bradycardia
< 60 bpm with regular rhythm
57
Sinus bradycardia is normal for what type of people
aerobically trained athletes (runners) people sleeping Beta blockers hypothyroidism *ask questions about why it could be so low*
58
Sinus bradycardia can occur in response to
parasympathetic nervous system carotid sinus massage Valsalva manuever hypothermia increase intraocular pressure vagal stimulation Beta blockers, Calcium channel blockers
59
Common diseases associated with sinus bradycardia
hypothyroidism increase intracranial pressure hypoglycemia inferior MI
60
S/S of Bradycardia
Hypotension Pale, cool skin Weakness Angina Dizziness or syncope Confusion or disorientation Shortness of breath
61
Tx for Bradycardia
**Atropine** Pacemaker Stop offending drugs (Hold, DC, or lower dose)
62
Symptomatic bradycardia is
a HR that is less than 60 beats/minute and is inadequate for the patient’s condition, causing the patient to experience symptoms
63
Atropine is what type of drug
anticholinergic (pt with symptoms)
64
Atropine for bradycardia (with symptoms) is
temporary fix and need to find a source
65
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.
- Shortness of breath. Rational : Signs of symptomatic bradycardia include pale, cool skin, hypotension, weakness, dizziness or syncope, confusion or disorientation, and shortness of breath.
66
Sinus Tachycardia is
normal sinus rhythm 101-180 bpm
67
Sinus tachycardia is associated with what physiologic and psychologic stressors including
exercise fever pain hypotension hypovolemia anemia hypoxia hypoglycemia MI HF hyperthyoidism anxiety fear
68
What drugs can cause sinus tachycardia?
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])
69
Will fluid bolus' help tachycardia patients?
yes
70
Tachycardia s/s
*depends on tolerance of the increased HR* Dizziness Dyspnea Hypotension - low CO Angina in patients with CAD
71
Tx of Tachycardia
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)
72
PSVT means
Paroxymal Supravntricular Tachycardia
73
PSVT is caused by
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
74
PSVT on EKG
absent P wave the faster it gets - hidden in preceding T wave - QRS interval is normal
75
PSVT bpm
151-220 (regular or slightly irregular)
76
PSVT occurs due to
reexcitation of the atria when there is a one-way block - PAC
77
Paroxysmal refers to
abrupt onset and ending
78
Paroxymal SVT followed by
brief period of asystole
79
PSVT is associated with
overexertion emotional stress deep inspiration caffeine and tobacco rheumatic heart disease dig toxicity CAD cor pulmonale
80
S/S of PSVT
HR is 150–220 beats/minute (add for clarification) HR > 180 leads to decreased cardiac output and stroke volume Hypotension Dyspnea Angina
81
PSVT with HR > 180 leads to
decreased CO and stroke volume
82
PSVT with HR > 180 s/s
Hypotension Dyspnea Angina
83
PSVT Tx
Vagal stimulation **IV adenosine (1st)** IV β-adrenergic blockers (sotalol) Calcium channel blockers (diltiazeem and amiodarone) Amiodarone DC cardioversion
84
What are common vagal stimulation manuevers tx for PSVT?
Valsalva, coughing, and or (Singing, Humming, and Gargling) -carotid massage only a doctor should perform this one.
85
Adenosine's half life is
short (10 seconds)
86
If vagal stimulation and drug therapy are ineffective for a PSVT and the patient becomes hemodynamically unstable, what should be used?
direct current cardioversion
87
Adenosine is what type of drug
antidysrhythmic
88
Adenosine for dx purpose can be used to
myocardial perfusion stress imaging study (vasodilator)
89
Adenosine for tx is used to
antidysrythmic for AVTs - gives the heart a break for the SA node to take back control
90
When giving adenosine you should tell the patient about feeling
chest pressure after the medication is given - injection in antecubital space close to the heart
91
How should adenosine be given?
IV rapid (1-2 secs) follow with 20mL flush rapid stop cock setup
92
What is the half-life of adenosine?
2-3 seconds
93
If the patient given adenosine has asystole after delivery what should the nurse do?
continue to monitor as asystole is normal
94
What equipment should a patient receiving adenosine have?
BP cuff 12 lead cardiac monitor defibrillator or AID ready
95
What should you assess for on a patient receiving adenosine?
flushing, dizziness, chest pain, or palpitation
96
What are the doses for adenosine?
6 mg 12 mg Stop after the second, HCP can continue - Cardioversion
97
Atrial flutter is 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
Atrial flutter means
atria is not emptying
99
Atrial flutter rates bpm
200-350
100
The ventricular rate of atrial flutter will vary based on
conduction ratio 2:1
101
The ventricular rate bpm in atrial flutter
150 bpm
102
In atrial flutter, the atrial and ventricular rythms are regular/irregular.
regular
103
Atrial flutter on EKG
P-R interval not measurable QRS normal **AV node delay signal to the atria - some AV block in fixed ratio
104
If the atrial flutter is not hemodynamically stable then what s/s or hx is seen?
cardiac hx medications chest pain SOB sweat
105
Atrial flutter is typically associated with
chronic lung disease, PE, cor pulmonale cardiomyopathy hyperthyoidism HTN CAD mitral valve disorders
106
What drugs can cause atrial flutter?
digoxin quinidine epinephrine
107
Patients with atrial flutter have an increased risk of stroke because
risk of thrombus formation in the atria from the stasis of blood
108
What is given to atrial flutter patients as a preventative of stroke
Warfarin
109
Tx of Atrial Flutter
Pharmacologic agent – anti-dysrhythmic Electrical cardioversion Radiofrequency ablation
110
The primary goal in treatment of atrial flutter is to
slow the ventricular response by increasing AV block
111
What drugs are used to slow down ventricular response in atrial flutter
Calcium channel and beta blockers
112
What is used to convert atrial flutter to sinus?
antidyrhythmic - ibutilide [Corvert] - amiodarone - flecainide [Tambocor] - dronedarone [Multaq]
113
If the patient is hemodynamically unstable with atrial flutter or they elect to have it, what can be used
electrical cardioversion
114
What is the treatment of choice for atrial flutter?
radiofrequency ablation - catheter in the r. atrium - low voltage and high frequency - tissue is destroyed and normal sinus rhythm restored
115
Atrial fibrillation causes the CO to
decrease = risk of stroke
116
Atrial fibrillation results in
decrease in CO because of ineffective atrial contractions (loss of atrial kick) and/or a rapid ventricular response
117
When the blood is stasis during a fib. =
clots form - pass into the brain causing a stroke
118
Paroxymal
spontaneous brief
119
Persistent lasts for
7 days +
120
A fib occurs in ___% of 65 + patients
6; increases with age
121
A fib occurs in what diseases
underlying heart disease, such as CAD, rheumatic heart disease, cardiomyopathy, hypertensive heart disease, HF, and pericarditis
122
Outside sources can cause a fib
acutely with thyrotoxicosis, alcohol intoxication, caffeine use, electrolyte disturbances, stress, and cardiac surgery
123
A fib is charcterized as
total disorganization of atrial electrical activity due to multiple ectopic foci resulting in loss of effective atrial contraction
124
Atrial rate during a fib
350-600 bpm
125
P waves in a fib
chaotic, fibrillatory waves
126
The ventricular rate of a fib is
irregular
127
The ventricular rate of someone with a fib with controlled ventricular response?
60-100 bpm
128
Atrial fibrillaion with rapid ventricular response rate is
>100 bpm (uncontrolled)
129
Tx for a fib.
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
The goal of a fib tx is to
decrease in ventricular repsonse <100 bpm prevent stroke conversion to sinus
131
What drugs are used for ventricular rate control in a fib patients?
calcium channel blockers beta blockers digoxin dronedarone
132
What drugs are most common for chemical cardioversion?
amiodarone and ibutilide
133
If a patient is in atrial fibrillation for longer than 48 hours, what is needed?
anticogulation therapy with warfarin for 3-4 weeks before cardioversion - clots dislodge = stroke
134
For patients with drug-refractory atrial fibrillation or who do not respond to electrical conversion what is used?
radiofrequency catheter ablation (similar to the procedure for atrial flutter) and the Maze procedure are further options.
135
The Maze procedure is a surgical intervention that
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
If the pateint has a fib start with
electrical cardioversion then drugs
137
If the patient has a SVT, start with
drugs then go to electrical cardioversion
138
PVCs are known as
mide, bizarre, QRS
139
PVC is a
contraction coming from an ectopic focus in the ventricles. It is the premature (early) occurrence of a QRS complex.
140
Multifocal means
different in shape PVCs
141
Unifocal PVC
PVCs remain the same
142
Ventricular bigeminy
every other beat is PVC
143
Ventricular trigeminy
every third beat is PVC
144
Couplet PVC
two consecutive PVCs
145
Ventricular tachycardia occurs when how many PVCS consecutive
3+
146
R-on-T phenomenon occurs
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
Excitability of the cardiac cells increase during
PVC - evolve into vent tachy or fibrillation
148
PVC rhythm
irregular - P wave rarely visible (lost in QRS)
149
Retrograde conduction
P wave is inside the ectopic beat - QRS distorted, prolonged, weird - T - large and opposite direction of QRS
150
If a hemodynamically stable patient has PVC, then
leave them alone
151
What should you use to treat a patient having numerous PVCs
lidocaine
152
PVCs are associated with
stimulants electrolyte imbalances hypoxia fever exercise emotional stress heart disease (MI, mitral valve prolapse, HF, and CAD)
153
PVC patients need to be assessed for
apical-radial pulse deficit
154
Tx for PVCs
Correct cause (O2 - hypoxia, replacement) assess hemodynamic state Antidysrhythmics - beta blockers, procainamide or amiodarone
155
What are stimulants for PVCs?
caffeine, alcohol, nicotine, aminophylline, epinephrine, isoproterenol, and digoxin
156
If a heart disease patient gets PVCs, then what will develop?
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
Ventricular Tachycardia is
3+ PVCs (Tombstones)
158
Ventricular rate of V Tach
150-250 bpm
159
AV ____________ may be present, with P waves occurring independently of the QRS complex IN V.Tach
dissociation
160
When V Tach is seen, what should you immediately do?
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
Polymorphic V Tach =
Torsades de Pointes
162
Torsades de Pointes means
twisting of the points
163
Torsades de Pointes is a deficit of
magnesium
164
With Torsades de Pointes, the nurse can give mag if
they know the mag level
165
Tx for Torsades de Pointe
code, CPR AND, defibrillate them Mag if know level
166
Ventricular Tachycardia pacemaker
ectopic foci (ventricles take over)
167
V Tach is considered life-threatening due to
decreased CO and the possibility of deterioration to ventricular fibrillation - low perfusion = hypoxic = unconscious
168
VT can quickly develop into
v fib
169
V Tach is associated with
heart disease (MI, CAD, significant electrolyte imbalances, cardiomyopathy, mitral valve prolapse, long QT syndrome) electrolyte imbalances drugs toxicity CNS disorder
170
Sustained Vtach causes
decrease in CO because of decreased ventricular diastolic filling times and loss of atrial contraction
171
Sustained V tach results in
hypotension, pulmonary edema, decreased cerebral blood flow, and cardiopulmonary arrest
172
Unstable V tach
pulseless
173
Stable V Tach
pulse
174
Stable V tach tx
VT with pulse (stable) treated with antidysrhythmics or cardioversion - IV procainamide, sotalol, or amiodarone
175
Unstable V tach Tx
CPR and rapid defibrillation vasopressors (epinephrine) antidyrhthymic (amiodarone)
176
If the VT is polymorphic with a normal baseline Q-T interval, any one of the following drugs is used:
β-adrenergic blockers, amiodarone, procainamide, or sotalol.
177
Polymorphic VT with a prolonged baseline Q-T interval is treated with
IV magnesium, isoproterenol, phenytoin (Dilantin), or antitachycardia pacing
178
dofetilide does what to QT interval
prolongs
179
V fib is a
severe derangement of the heart rhythm characterized on ECG by irregular waveforms of varying shapes and amplitude
180
V fib is firings of
multiple ectopic foci in the ventricle. Mechanically the ventricle is simply “quivering,” with no effective contraction, and consequently no CO occurs **chaotic squiggles**
181
In v fib, what is the heart rate
not measurable
182
V fib is associated with
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
V fib patients are usually
unresponsive, pulseless, and apneic state.
184
Tx for v fib
with immediate CPR and ACLS Defibrillation ACLS Drug therapy (epinephrine, vasopressin)**
185
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.
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
Asystole represents
total absence of ventricular electrical activity - no depolarization = no contractions
187
Asystole patients are found
**unresponsive, pulseless, and apneic**
188
With asystole patients check the rhythms in
all leads
189
Tx of Asystole
**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
Asystole result in
advanced cardiac disease, severe conduction disturbance, or end-stage HF - prolonged arrest usually not able to be resuscitated
191
PEA
Electrical activity can be observed on the ECG, but no mechanical activity of the ventricles is evident, and the patient has no pulse
192
PEA has no
mechanical movement of the heart - poor prognosis unless cause is tx
193
The most common causes of PEA Hs and Ts
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
Treatment for PEA
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
Third-Degree AV Heart Block
complete heart block, constitutes one form of AV dissociation in which no impulses from the atria are conducted to the ventricles
196
Third-Degree AV Heart Block is caused by what in the heart
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
Third-Degree AV Heart Block - atrial rate AV
40-60 bpm
198
Third-Degree AV Heart Block - Purkinje fibers rate
20-40 bpm
199
Third-Degree AV Heart Block is associated with
severe heart disease (CAD, MI, myocarditis, cardiomyopathy, some systemic diseases (amyloidosis, scleroderma, certain drugs (digoxin, β-adrenergic blockers, and calcium channel blockers)
200
Third-Degree AV Heart Block usually results in
decreased CO
201
Third-Degree AV Heart Block leads to
syncope, HF, shock - severe bradycardia to periods of asystole
202
Third-Degree AV Heart Block Tx
symptomatic - permanent trancutaneous pacemaker ASAP
203
Temporary Tx for Third-Degree AV Heart Block
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
Isoelectric line is
flat and represents those normal times in the cardiac cycle when the ECG is not recording any electrical activity in the heart
205
St-segment elevation associated with
myocardial injury (STEMI) - Q wave is prolonged - R is elevated and prolonged - tx cath lab within 90 minutes
206
ST segment depression and T inversion is in a
NSTEMI - tx medically
207
Biphasmic Defibrillation joules
120-200 J
208
Monophasmic Defibrillation joules
360 J
209
After the first shock of defibrillation,
start CPR immediately beginning with chest compressions. - give it time to go back to rhythm
210
Cardioversion needs to
sync with Q waves for shock
211
Cardiac Pacemaker
electronic device used to pace the heart when the normal conduction pathway is damaged - control heart rate with compromised conduction
212
Single chamber pacemaker
either atria or ventricles
213
Dual chmaber pacemaker
paces both atrium and ventricles
214
Capture measn
electrical charge produces atrial or ventricular contraction
215
Sensed
recognize spontaneous atrial or ventricular activity
216
Permanent Pacemaker is
implanted
217
Temporary Pacemaker
power source outside the body - transvenous, epicrdial, trancutaneous
218
Trancutaneous Pacemakers
noninvasive, temporary procedure used until a transvenous pacemaker is inserted or until more definitive therapy is available
219
Where do you place the pads for defibrillation?
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
Failure to sense occurs
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
Failure to capture
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
What are the lethal dysrhythmias?
Vtach Vfib Asystole 3 degree Heart Block
223
What are shockable rhythms?
V tach and v Fib
224
Rhythms that can cardiovert
SVT Afib Aflutter
Module 7 (Critical Care)
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Decks in class (22)
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