APEX Monitoring III: CARDIAC RHYTHMS Flashcards
1
Q
Which pathway depolarizes the LA?
A
Bachman bundle
2
Q
What are 3 internodal tracts that travel from the SA node to the AV node
A
Bachmann bundle
Wenckebach tract
Thorel tract
3
Q
Kent’s bundle is a
A
Pathologic accessory pathway that is responsible for Wolf Parkinson-White syndrome.
4
Q
Cardiac Conduction system contains:
A
SA node Internodal tracts AV node Bundle of HIS Bundle Branches Purkinje fibers
5
Q
3 internodal tracts
A
Anterior Internodal tract
MIddle Internodal tract
Posterior internodal tract
6
Q
The anterior internodal tract is the
A
Bachmann bundle
7
Q
The middle internodal tract
A
Wenckeback tract
8
Q
The posterior internodal tract
A
Thorel tract
9
Q
Conduction velocity quantified
A
how fast an electrochemical impulse propagates along a neural pathway.
10
Q
Conduction velocities of the cardiac conduction pathway : SA and AV nodes
A
0.02 - 0.1 m/sec (slow conduction )
11
Q
Conduction velocities of the cardiac conduction pathway : HIS bundle, bundle branches and purkinje fibers
A
1-4 m/sec (fast conduction)
12
Q
Conduction velocities of the cardiac conduction pathway : MYOCARDIAL MUSCLE CELLS
A
0.3 - 1 m/sec (intermediate)
13
Q
Conduction velocity is a funciton of
A
Resting membrane potential
Amplitude of the action potentila
Rate or change in membrane potential during phase O
14
Q
Conduction velocity is affected by
A
ANS tone Hyperkalemia induced closure of fast Na+ channesl Ischemia Acidosis Antiarrhythmic drugs
15
Q
There is a band of connective tissue that electrically isolates the atria from the
A
ventricles.
16
Q
What is the only electrical pathway between the cardiac chambers?
A
AV node
17
Q
AV node is the
A
Gatekeeper of electrical transmission between the atria and the ventricles.
18
Q
Accessory Pathway : James Fiber
A
Connect Atrium to AV node
19
Q
Accessory Pathway : Atria HIsian Fiber
A
Connect Atrium to HIs bundle
20
Q
Accessory Pathway : Kent’s Bundle
A
Connect Atrium to Ventricle
21
Q
Accessory Pathway : Mahaim Bundle
A
AV node to ventricle
22
Q
What are the 5 phases of the ventricular action potential
A
0 , 1, 2, 3, 4
23
Q
Phase O is
A
Rapid depolarization (QRS)
24
Q
Phase 1 is the
A
Initial repolarization (QRS)
25
Phase 2 is the
plateau phase (QT interval)
26
Phase 3 is the
Final repolarization (T Wave)
27
Phase 4 is the
Resting phase (T -> QRS)
28
Depolarization Na+ movement
In
29
Initial repolarization ion movement
Cl- --> in
| K+ --> out
30
Plateau movement ion movement
Ca2+ in
| K-> Out
31
Final repolarization ion movement
K + out
32
Resting phase ion movement
Na+ Out
33
What is the ABSOLUTE REFRACTORY period?
No stimulus (no matter how strong) can depolarize the myocyte.
34
What is the RELATIVE REFRACTORY period?
Larger than normal stimulus required to depolarize the myocyte.
35
EKG event: P Wave : Electrical event in ATRIA and ventricle
Atria: depolarization begins
| Ventricles; NONE
36
EKG event: PR INTERVAL: Electrical event in ATRIA and ventricle
Atria: Depolarization complete
Ventricles: NONE
37
EKG event:QRS : Electrical event in ATRIA and ventricles
ATRIA: Repolarization
Ventricles: Depolarization begins
38
EKG event: ST segment : Electrical event in ATRIA and ventricle
ATRIA:NONE
VENTRICLES: DEPOLARIZATION complete
39
EKG event: T Wave : Electrical event in ATRIA and ventricles
ATRIA: NONE
VENTRICLES: Repolarization begins
40
EKG event: after T Wave : Electrical event in ATRIA and ventricl
Atria: NONE
| REPOLARIZATION complete
41
EKG signs of Pericarditis
PR interval depression
42
EKG signs of HYPOKALEMIA
U wave
43
EKG signs of Intracranial hemorrhage
Peaked T wave
44
EKG signs of WPW syndrome
Delta wave
45
Duration of P wave in sec____
0.08-0.12
46
Amplitude of P wave in mm
< 2.5
47
Prolonged with 1st degree HB
P wave
48
PR intervanl normal
0.12 -0.20 sec
49
Q wave when to consider MI
Amplitude is greater than 1/3 R wave
Duration is greater than 0.04 seconds
Depth is greater than 1 mm
50
Normal QRS is
<0.10
51
Normal QRS amplitude progressively
increase from V1-V6, normal R wave progression.
52
If QRS complex if increased consider
LVH
BBB
Ectopic beat
WPW
53
QTc interval normal value in men
< 0.45
54
QTc interval normal value in women
< 0.47
55
ST segment when to consider MI
ST elevation or depression greater than 1 mm
56
ST elevation also caused by (other than the obvious MI)
Hyperkalemia
| Endocarditis
57
T wave amplitude should be in precordial leads
Less than 10mm
58
T wave amplitude should be in limb leads
Less than 6 mm
59
Usually T wave points in the
Same direction as QRS
60
When T wave point in opposite direction of QRS
if repolarization is prolonged by MI, BBB
61
Peaked T waves are caused by
MI
LVH
Intracranial bleed
62
U wave if greater than
1.5mm, consider HYPOKALEMIA
63
Where is the J point ?
The point where the QRS complex and the ST segment begins.
64
By measuring the J point, relative to the PR segment we can
quantify the amount of ST elevation and depression
65
High potassium on T, QT, QRS
| Early to late signs
```
Narrow peaked T
Short QT
Wide QRS
Low P amplitude
Wide PR
Nodal BLOCK
Sine wave fusion of QRS and T --> VF or asystole.
```
66
Too low potassium on QT
Long QT interval
67
Hypercalcemia on QT
Short QT
68
Hypocalcemia on QT
Long QT
69
Very low mag on QT
Long QT
70
The waveform on the EKG is a measure of the
Mean electrical vector
71
2 vectors to understand
Vector of depolarization
| Vector of repolarization
72
Each lead consist of
One negative electrode
| One positive electrode
73
Vector of depolarization
QRS complex
74
Direction the heart
Depolarizes from 1, base =>apex and 2. Endocardium--> Epicardium
75
Polarity the myocytes go from
internally (-) to internally (+) THIS PRODUCES A POSITIVE ELECTRICAL CURRENT
76
When does a positive deflection occur?
when the vector of depolarization TOWARDS the positive electrode.
77
When does a negative deflection occur?
when the vector of depolarization AWAY from the positive electrode.
78
When does a BIPHASIC deflection occurs?
when the vector of depolarization PERPENDICULAR to the positive electrode.
79
Vector of REPOLARIZATION
T wave
80
Direction the heart repolarizes form
1. apex --> Base and 2. Epicardium --> Endocardium
81
Think of repolarization as the
Opposite of depolarization
82
Polarity the myocytes from internally (+) to internally (-) this produces a
Negative electrical current
83
A positive deflection occurs when the wave travels
AWAY from the positive electrode
84
The vector of repolarization travels in the
Opposite direction as the vector of depolarization
85
The vector of repolarization produces a
negative current
86
12 leads are
12 cameras
87
How many bipolar leads
3
88
How many limb leads
3
89
How many precordial leads
6
90
What are the bipolar leads
I, II, III
91
What are the limb leads
aVR
aVL
aVF
92
What are the precordial leads
```
V1
V2
V3
V4
V5
V6
```
93
Septum leads are
V1, V2
94
Anterior leads are
V3, V4
95
Lateral leads are
I, aVL, V5, V6
96
Inferior leads are
II, III, aVF
97
The mean electrical vector tends to point to
Towards areas of hypertrophy (more tissue to depolarize)
| Away from areas of Myocardial infarction (The vector must travel around these areas)
98
The mean electrical vector normal value is between
-30 degrees and +90 degrees
99
Axis represents the
direction of the mean electrical vector in the frontal area.
100
Examine those 2 leads to determine axis
I and aVF
101
Normal axis: I and AVF
Both positive
102
Left axis deviation
Lead I positive
| Lead avF negative
103
Right axis deviation
Lead I negative
| Lead avF positive
104
Extreme Right axis deviation
Lead I and avF negative
105
Leads reaching toward each other then we have (l pointing down and avF pointing up)
Right axis deviation
106
Leads Leaving each other (L pointing up and avF pointing down_ then we have
LEFT AXIS deviation
107
Left axis is more
more negative than -30 degrees
108
Right axis is more
More positive than 90 degrees.
109
Axis deviation with COPD
Right
110
Axis deviation with chronic HTN
Left
111
Axis deviation with Acute bronchospasm
Right
112
Axis deviation with Cor pulmonale
Right
113
Axis deviation with Pulmonary HTN
Right
114
Axis devation with PE
right
115
Axis deviation with LBBB
Left
116
Axis deviation with Aortic stenosis
Left
117
Axis deviation with aortic insuffieciency
Left
118
Axis deviation with mitral regurgitation
Left
119
Adenosine is an
Endogenous nucleoside slows the conduction through the AV node.
120
ACtion of adenosine
Stimulate the cardiac adenosine-1 receptor , adenosine activates K currents, which hyperpolarizes the cell membrane and reduces action potential.
121
2 things Adenosine good for
SVT
| WPW
122
Adenosine effective in treating Afib?
No
123
Adenosine effective in treating Aflutter?
No
124
Adenosine effective in treating Torsdades de pointes
No
125
Lidocaine class
IB
126
Amiodarone Class
III
127
Beta Blocker antiarrythmic class
Class II
128
CCB antiarrythmic class
Class IV.
129
Class I drugs inhibit
fast sodium channels
130
Class II drugs decrease the
rate of depolarization
131
Class III drugs inhibit
Posstaium ion channels
132
Class IV drugs inhibit
Slow calcium channels.
133
Sinus arrhythmia occurs when the
SA note pacing rate with respiration. its usually benign
134
What is the Bainbridge reflex?
When an increased in venous return stretches the RA and SA node causing the HR to increase. It should make sense that it would cause sinus arrythmia.
135
Inhalation effect on on intrathoracic pressure?
Decrease intrathoracic pressure --> Increase VR and increase HR.
136
Exhalation effect on on intrathoracic pressure?
Increase intrathoracic pressure --> Decrease VR and decrease HR.
137
SInus bradycardia defined as
HR < 60
138
What is the most common source of bradycardia?
Increased vagal tone.
139
What is the first line of Tx for bradycardia?
Atropine.
140
What can cause paradoxical bradycardia with atropine? Mediated by?
Underdosing it < 0.5mg IV. Presynaptic muscarinic receptors.
141
Severely symptomatic patients with bradycardia should receive
Immediate transcutaneous pacing.
142
Beta Blocker or CCB overdose treatment.
GLUCAGON
143
How does glucagon work ?
Stimulating glucagon on the myocardium. INCREASING cAMP leading to increase HR, contractility, and AV conduction.
144
What is the initial dose of glucagon?
50-70mcg/kg q3-5 min, can be FOLLOWED By infusion at 2-10 mg/hr
145
What causes tachycardia?
Increase intrinsic firing rate of the SA node or sympathetic stimulation.
146
Some etiologies of tachycardia
Hypovolemia, hypoxemia, infection. MH, Thyrotoxicosis
147
What is the effect of tachycardia on oxygen balance?
Increase myocardial oxygen demand WHILE decreasing oxygen supply.
148
Tachycardia can precipitate what ?
MI and CHF in patients with POOR CARDIAC RESERVE>
149
Tachycardia and patients with CAD
Precipitate MI and/or infarction
150
Best initial treatment of tachycardia
Treating the underlying cause
151
Best 2nd treatment of tachycardia
rate control with Bblockers or CCBs.
152
AFib is an
irregular rhythm with the absence of a P wave
153
With Afib, Chaotic electrical activity in the
Atrium is conducted to the ventricle at a varied and irregular
154
Afib and effect on CO
LOSS OF ATRIAL kick
155
Afib and perioperative mortality
Increase risk
156
Main problem with afib is
Risk of atrial thrombus formation (risk of stroke)
157
Afib with RVR
reduces diastolic filing time and is ASSOCIATED WITH severe reduction in CO
158
Afib with RVR associated with severe reduction of CO as manifested by
syncope
chest pain
SOB
159
2 Treatments of Afib with RVR
Beta blockers, CCB, Digoxin
| AND anticoagulation
160
Acute onset of Afib treated with
Cardioversion (start at 100Joules)
161
AFIB onset and its implications
If onset is older than 48 hours (or if onset is undertermined) a TEE must be performed to rule out atrial thrombus.
162
Arrhythmia that is an indication to cancel surgery
new onset afib; aflutter
163
What is the most COMMON POSTOP tachydysrhythmia? when does it usually occurs and who is at risk?
Atrial fibrillation ; 2-4 days'' older patients post CT surgery.
164
Aflutter compared to afib is
Organized supraventricular rhythm
165
Aflutter is recognizable with what kind of pattern.
Saw tooth pattern
166
In aflutter what is the atrial rate
250-350
167
During a flutter , each atrial depolarization produces an
Atrial contraction , but not all atrial depolarizations are conducted past the AV node.
168
Usually defined with AFLUTTER
Defined ration of atrial to ventricular contractions.
169
In atrial flutter, what prevents all impulses from being transmitted to the ventricles?
Effective refractory period.
170
If atrial flutter onset is older than 48 hours or unknown?
TEE must be performed to r/o atrial thrombus.
171
Risk with RVR
can lead to hemodynamic instability
172
Treatment of aflutter
Rate control or cardioversion
173
Hemodynamically unstable atrial flutter should be treated with cardioversion start at
50 Joules
174
PVC originated from Foci b
Below the AV node, such as the QRS complex is wide
175
PVCs that arise from a single location are
unifocal (the morphology is the same on the EKG)
176
PVCs that arise from multiple location are
Multifocal (different QRS morphologies on the EKG)
177
Electrolytes disturbances associated with PVCs
Hypomagnesemia
| Hypokalemia
178
Heart issues associated with PVCs
MI or infarction
SNS stimulation (acidosis, Hypercabia, hypoxia)
Valvular disease
Cardiomyopathy
179
Associated with PVCs other factors
Caffeine
Cocaine
Alcohol
180
A PVC that lands on the
2nd half of the T wave meaning during the relative refractory period can precipitate the R on T phenomenon
181
PVCS should be treated when?
Frequent > 6 /min polymorphic or occurs in runs of 3 or more
182
Treatment of PVCs
reverse underlying cause
| Repositioning central line that may be irritating the RA
183
Medication treatment of PVCs
Treated with LIDOCAINE 1-1.5 mg/kg. if not resolved follow by infusion 1-4 mg/min
184
What is BRUGADA Syndrome?
Sodium ion channelpathy in the heart.
185
What can BRUGADA syndrome cause?
Sudden nocturnal death due to Vtach or fibrillation
186
Brugada most common in males from
SOUTHEAST asia
187
BRUGADA syndrome Diagnosis EKG findings include a
RBBB and ST segment elevation in V1-V3
188
Pt with BRUGADA syndrome may require
ICD or pad placement during surgery.
189
First degree HB : THE PRI is
>0.20 second
190
Affected regions in first degree
AV node or HIS bundle
191
Etiology of HB
Age related degenrative changes, CAD, digoxin and amiodarone.
192
Treatment of HB
Monitor (usually asymptomatic)
193
Longer, longer, longer, drop then you have a
Wenckebach (2nd degree type I HB)
194
PR interval In 2nd degree HB type I
The PR interval becomes progressively long with each cycle, but the last P wave does not conduct to the ventricles, then the cycle repeats.
195
Why does the PR gets longer with a 2nd degree HB type I
Each successive depolarization increases the duration of the refractory period in the AV node. The last P in the cycle dropped, because it arrives at the AV node while it's in the ABSOLUTE refractory period. This beat is not conducted but the pause that follows provides enough time for the AV node to reset. Then the cycle repeats.
196
Affected region in 2nd degree HB type I
AV node.
197
Etiology in 2nd degree HB type I
structural conduction defect, MI, BBlockers, CCBs, digoxin, sympatholytics agents.
198
Treatment of 2nd degree HB type I
Asymptomatic: just monitor
Symptomatic: then GIVE ATROPINE
199
2nd degree HB Block (Mobitz type II) if some Ps dont get through then you have a
Mobitz II
200
2nd degree HB Block (Mobitz type II) Some Ps conduct to the ventricles, while
Others don't (there is usually a set ratio 2:1 or 3:1. After the dropped QRS the next P arrives right on time.
201
Affected region on 2nd degree HB Block Mobitz type II.
HIs bundle or bundle branche
202
Etiology in 2nd degree HB Block Mobitz type II
structural conduction defect or infarction .
203
Treatment of 2nd degree HB Block Mobitz type II
Often symptomatic
Pacemaker
atropine often not effective.
204
Key point of 2nd degree HB Block Mobitz type II
HIGH RISK OF PROGRESSING TO COMPLETE HB>
205
If Ps and Qs dont agree then you have
3rd degree.
206
AV dissociation with atria and ventricles have their onw rates
Third degree HB
207
With 3rd degree HB block in the AV node has a
narrow QRS (rate 45-55bpm)
208
With 3rd degree HB block Below the AV node has a
wide QRS (rate 30-40)
209
Etiology of 3rd degree HB
Fibrotic degeneration of the atrial conduction system. Lenegre's disease.
210
Treatment of 3rd degree HB
PM
| ISOPROTERENOL (chemical PM)
211
3rd Degree HB symptoms
Often symptomatic: syncope, dyspnea, weakness, vertigo.
212
Key points about 3rd degree HB symptoms
Can lead to CHF due to decreased HR and CO
213
Stokes-Adams attack is associated with
3rd degree HB
214
What is STOKES-ADAMs ATTaCK?
Decreased CO --> Decrease cerebral perfusion --> Syncope
215
How are antiarrhythmic drugs are classified according to their ability to
Block specific ion channels and currents of the cardiac action potential
216
Mechanism of action of CLASS IA
Moderate depression of phase O
| Prolongs phase 3 repolarization (K+ channel block --> Prolonged QT )
217
Class I anti-arhythmic action on what 2 phases
Phase 0 and Phase 3
218
Mechanism of action of CLASS IB
Weak depression of phase O
| Shortened phase 3
219
Examples of Class IA
Quinidine
Procainamide
Disopyramide
220
Examples of Class IB
Lidocaine, Phenytoin
221
Mechanism of action of CLASS IC
STRONG depression of phase O
| Little effect on phase 3 repolarization
222
Examples of Class IC
Flecainide, Propafenone
223
Class 2 are the
Beta Blockers
224
Mechanism of action of Beta Blockers
Slows phase 4 depolarization in SA node
225
Class III are the
K+ Channels
226
Mechanism of action of K+ Channel Blockers (Class III)
Prolongs Phase 3 repolarization (prolonged QT)
| Increase ERP
227
Class IV are the
Ca2+ Channel blockers
228
Mechanism of action of Ca2+ CCB
Decrease conduction through the AV node
229
How is adenosine metabolized
Plasma
230
Half time of adenosine
5 seconds
231
Adenosine useful for
SVT
| WPW with a narrow QRS
232
Adenosine and reactive airway
Bronchospasm in asthmatic patients.
233
How to dose adenosine? Peripheral IV
First dose: 6mg
| Second dose : 12 mg if required
234
How to dose adenosine? Central line
First dose: 3 mg
| Second dose: 6mg
235
WPW is associated with : what kind of re-entry
Atrial -ventricular reentry
236
When does WPW occurs?
When an accessory pathway joins the atrium to the ventricle: called Kent's Bundle
237
Most common cause of tachyarrythmias are
Reentry pathways
238
Explain the impulse conduction through the normal pathway?
SA node --> AV node --> HIS bundle --> Bundle branches---> purkinje fibers
239
Can impulse move backwards?
No because all the tissues behind the impulse remain in the absolute refractory period
240
What is the ratio of SA node depolarization and cardiac contraction?
1:1
241
Single pathway conduction system: how does it occur?
As the cardiac impulse propagates, it may encounter an area that can create an electrical circuit. It will travel along both pathways. Left and right at the same speed. Meet in the middle and cancel each other out.NO opportunity for reentry.
242
What is reentry?
single cardiac impulse can move backwards and excite the same part of the myocardium over andover.
243
Ratio of SA node discharge and cardiac contraction can exceed 1:1 ratio, there is a risk that
an impuse that circles around the reentry pathway will precipitate a reentry tachyarrhythmia.
244
How to break a circuit for reentry? 2 ways
Slowing down conduction velocity through the circuit
| Increasing the refractory period of the cells at the location of the unidirectional block
245
3 possible causes of reentry?
Conduction occurs over a long distance
Conduction velocity is too slow
Refractory period is shorter.
246
Example of conduction over a long distance
Left atrial dilation due to mitral stenosis
247
Example of conduction velocity is too slow
Ischemia
| Hyperkalemia
248
Refractory period is shorter example
Epinephrine
| Electric shock from alternating current.
249
Patient with WPW develops afib during surgery , 2 medications to give
Procainamide
| Amiodarone
250
What is the most common pre-excitation syndrome?
WPW
251
Defining feature of WPW
Consists of an accessory conduction pathway that bypasses the AV node (Kent's bundle)
252
The accessory pathway forms a direct line of communication between the atrium and the ventricel
Kent's bundle
253
During the normal conduction pathway, the cardiac impulse is delayed where?
At the AV node, meaning the AV node has a long refractory period.
254
What happens during the accessory pathway?
There is not delay , impulse move quickly from the atrium to the ventricle. There is no gatekeeper function .
255
How is WPW Diagnosed?
routine EKG , or hx of tachydysrhythmias.
256
Characteristicts of WPW on EKG
***Delta wave
***Short PR < 0.12 second
***wide QRS complex
possible t wave inversion
257
Why is there a delta wave?
Because of ventricular preexcitation.
258
WPW syndrome is classified in
Type A and type B.
259
WPW type A
right bundle branch block with right ventricular hypertrophy
260
WPW Type B
resembles left bundle branch block with left ventricle hypertrophy.
261
Most common tachydysrhythmia associated with WPW?
AV nodal reentry tachycardia
262
AV nodal reentry tachycardia classified as
Orthodromic or antidromic
263
Orthodromic vs antidromic: more common
Orthodromic (`90% cases) Antidromic (10% of cases)
264
Reentry conduction pathway with orthodromic
Atrium --> AV node --> Ventricle--> Accessory pathway ---> Atrium
265
Reentry conduction pathway with antidromic
Atrium --> Accessory pathway ---> Ventricle--> AV node --> ATrium
266
QRS morphology with orthodromic
Narrow
267
QRS morphology with antidromic
Wide
268
QRS in orthodromic: what happens with ventricular depolarization?
Normal via the HIS- Purkinje system
269
QRS in antidromic: what happens with ventricular depolarization?
Ventricular depolarization is slower since HIS system is bypassed.
270
Goal of Treatment of orthodromic
Block conduction at the AV node pathway (Increase the AV node refractory period)
271
Block conduction at the AV node pathway for orthodromic treatment include
```
Vagal maneuvers
Amiodarone
Adenosine
BBlockers
Veraparmil
Cardioversion
```
272
Goal of Treatment of antidromic:
Block conduction at the accessory pathway (Increase accessory pathway refractory period)
273
Block conduction at the accessory pathway with those treatment for antidromic
Procainamide
Amiodarone
Cardioversion .
274
Do not do this with antidromic pathway?
Do not give agents that increase the refractory period of the AV node, because doing so will favor conduction through the accessory pathway.
275
Orthodromic vs antidromic which one is more dangerous?
Antidromic
276
Why is antidromic more dangerous?
Because the gatekeeper function of the AV node is bypassed and the HR can increase well beyond the heart's pumping ability (dramatically reduces filling time)
277
If you give an AV nodal blocking drug to a patient with antidromic AVNRT what will happen?
You will force the conduction along the accessory pathway. This can induce Vfib. THEREFORE avoid drugs that BLOCK CONDUCTION through the AV node.
278
Drugs to AVOID with antidromic AVNRT include
```
Adenosine
Digoxin
CCBs (Diltiazem and verapamil)
BBlockers
Lidocaine.
```
279
Safe opitions for both orthodromic and ANTIDROMIC AVNRT?
Amiodarone
| Cardioversion
280
Afib and WPW : Because there is no delay in the accessory pathway,
A rapid atrial rate can be conducted to the ventricles in a 1:1 ration .
281
During atrial fibrillaiton , the atria can depolarize up to
300x per minutes.
282
Combination of AF and WPW can precipitate 3 thins
CHF
Vfib
Death .
283
Why is Procainamide the tx of choice for WPW?
It increases the REFRACTORY PERIOD in the accessory pathway.
284
IF the patient is hemodynamically unstable,best option is
Cardioversion
285
What is the definitive treatment for accessory pathway?
Radiofrequency ablation
286
Risk with radiofrequency ablation of pathways involving the Left atrium?
Imposes a risk of thermal injury to the left atrium and the esophagus.
287
What is required when there is ablation of a pathway involving the left atrium?
Esophageal temperature is required.
| If the temperature rises during periods of ablation, YOU MUST INFORM THE CARDIOLOGIST IMMEDIATELY.
288
Increases the likelihood of torsades de pointes in the patient with Long QT syndrome 3 things
Furosemide
Hyperventilation
Methadone
289
Patients with long QT syndrome at risk for
Torsades de pointes.
290
Patients with long QT syndrome should not receive
Methadone
291
The only narcotic known to increase the QT interval
Methadone
292
Furosemide and QT interval
Can cause hypokalemia and hypomagnesemia which can further prolong the QT interval
293
Hyperventilation and QT
Hyperventilation shifts K+into cells, decreases serum K and prolong the QT interval
294
Twisting of the spikes
Torsades de pointes.
295
Underlying cause of torsade de pintes?
Delay in ventricular repolarization (phase 3 of the action potential). se
296
Torsades de pointes is ______But can deteriorate to
Self limiting; ventricular fibrillation.
297
Torsades de pointes QT
Torsades associated with long QT
298
Causes of torsade de pointes mnemonic
```
Phenothiazines
Other meds
Intracranial bleed
No known cause
Type I antiarrythmics
Electrolytes disturbance
Syndromes
```
299
Antiemetic drugs causes Long QT
Haloperinol
Droperinol
Ondansetron
300
Antiarrhythmic causing prolonged QT
Amiodarone (especially with hypokalemia)
| Quinidine
301
Genetic syndromes associated with Prolonged QT
Romano-ward syndrome
| Timothy syndrome
302
QT interval and HR
Inversely related with HR.
303
Prolonged QT parameter in men
>0.45 seconds
304
Prolonged QT parameter in women
>0.47 seconds
305
Other text consider QT _______ prolong
>40 seconds
306
PVC or poorly timed pacer discharge during the
relative refractory periods (during the second half of the T wave) can cause torsades pointes. (R on T phenomenon)
307
Prevention and treatment: Patients with Long QT syndrome may require
Beta blocker prophylaxis and /or ICD placement
| Avoid SNS stimulation
308
Acute treatment for torsades de pointes include
Reversing the UNDERLYING cause and/or shorten the QT interval.
309
Acute treatment of torsades de pointes with meds
Magnesium sulfate
| Cardiac pacing to increase th HR will reduce the action potential duration and the QT interval.
310
Pacemaker Position I is
Chamber PACED
311
Pacemaker positionII is
Chamber SENSED
312
Pacemaker position III is
Response to sensed event
313
Pacemaker position IV is
Programmability
314
PM mnemonic for position
PaSeR
315
When is a pacemaker required?
Heart unable to produce a normal rate and rhythm.
316
3 major indications for pacemaker
Long QT syndrome
Dilated cardiomyopathy
Hypertrophic obstructive cardiomyopathy
317
Major indications for pacemaker nodal issue
Symptomatic diseases of impulse formation (SA node disease or AV node disease
318
What does a pacemaker consistst of
Pulse generator and pacing leads that deliver electrical current to the heart.
319
Epicardial leads function
stimulate the surface of the heart.
320
Transvenous lead function
stimulated the cardiac chambers (RA and or RV)
321
Position I can be one of 4
O=none
A=Atrium
V= Ventricle
D= Dual
322
Position II can be one of 4
O=none
A=Atrium
V= Ventricle
D= Dual
323
Position III can be one of 4
T= Sensed activity tells the pacemaker to fire
I = Sensed activity tells the pacemaker NOT to fire
D-= if native activity is sensed , then pacing is inhibited
If native activity is not sense, then the pacemaker fire.
324
Position III can be one of 4
None
triggered
Inhibited
Dual(D+T)
325
Position IV can be one of 2
```
O= none
R= rate modulation
```
326
None or rate modulcaiton indicates the
programmability of the pacemaker. ability to adjust HR in response to physiologic need. Sensors can measure respiration, acid base status,vibration,etc.
327
Position V indicates that
The PM can pace multiples sites.
328
This mode improves AV synchrony
DDD
329
This of this as a bckup mode: only fires when the native heart rate fails belowa predetermined rate
Single-Chamber demand pacing
330
This of this as a bckup mode: only fires when the native heart rate fails belowa predetermined rate
Single-Chamber demand pacing : AAI, VVI
331
This mode makes sure that the atrium contracts first followed by the ventricle
Dual-chamber AV sequential Demand Pacing (DDD)
332
There is no sense or inhibition with this mode
Asynchronous pacing
333
There is no sense or inhibition with this mode
Asynchronous pacing AOO, VOO, DOO
334
IF the atrium is paced, what happens to the electrical signal>
Travels through the AV node and the QRS maintain its normal , narrow appearance.
335
IF the ventricle is paced, what happens to the electrical signal>
is delivered beyond the AV node and the QRS takes on a WIDE APPEARANCE>
336
The pacemaker can fail to capture because of
hypocarbia (which can cause HYPOKALEMIA) made the myocardium more resistant to depolarizaiton.
337
Types of scapel that decreases the chance of EMI
Ultrasonic Harmonic Scapel.
338
Electrocautery that reduces the risk of EMI
Changing from coagulation to cutting
339
Hypothermia and HR
Bradycardia
340
MAGNET role : placing a magnet over the device does what?
Converts the PACEMAKER to an asynchronous mode.
341
The best answer for magnet is to
consult with the manufacture to determine how a magnet affects the pacemaker.
342
Magnet over an ICD
Suspends the ICD and prevents shock delivery
343
PM and ICD magnet
Suspeds the ICD and prevents shock delivery
| Has no effect on the PM function (PM will be subject to EMI)
344
How to minimize the risk of PM failure
1. Pulse generator failure
2. Lead failure
3. Failure to capture.
345
Risk of EMI is the greatest with the use of
Electrocautery and radiofrequency ablation.
346
Monopolar vs bipolar cautery?
Monopolar causes more EMI than bipolar
347
If surgeon insists of monopolar cautery
Insist on short bursts (0.5 seconds)
348
The risk of EMI is highest when
the electrocautery tip is used within a 15 cm radius of the pulse generator
349
Conditions that may cause PM to fire but there may be a failure to capture?
Hyper and hypokalemia
Hypocapnia
Hypothermia
MI
350
MRI contraindicated
PM or ICD
351
Lithotripsy and PM
LIthotripsy is not contraindicated, beam should be directed away from the pulse generator.
352
ECT and PM
ECT not contraindicated.
353
Not a reason to avoid this med with PM
Succinylcholine
354
The single most important informationto know preoperatively when the pacemaker fails?
Preoperatively find out what the patient's underlying rhythm is .
Consider isoproterenol, Epinephrine and/or atropine.
355
K+ and conditions that can affect PM
Hyper and hypokalemia
356
4 others conditions that can affect PM
```
Hypocapnia (Intracellular K shift)
Hypothermia
MI
Fibrotic tissue buildup around the pacing leads
Antiarrhythmic medications.
```
357
Hyper/hypocalcemia with QT
Hyper makes it shorter , hypo makes it longer.
358
When QT at risk for torsades
When longer than >0.5 seconds
359
What is the lead that is always positive
LEFT LEG
360
What is the lead that is always negative
RIGHT ARM
361
Left AXIS Deviation is
362
Right AXIS deviation is
>90 degrees
363
What is the MOST COMMON CAUSE of ACUTE MI
Sinus tachycardia (because it simultaneously increases myocardial oxygen demands while decreasing O2 supply.
364
3 meds for a flutter
Amiodarone
Diltiazem
Verapamil
365
PVCs causes by
Digoxin toxicity
| Hypokalemia
366
Best drug for the treatment of symptomatic PVCs
Lidocaine.
367
Safest to administer to a patient with prolonged QT syndrome?
Metoprolol
368
Genetic disorder linked to MH
King DENBOROUGH
369
2 potential causes of 1st degree HB
Amiodarone
| Advanced age
370
Reference point for measuring changes in the ST segment is
PR segment
371
Adenosine best in the treatment of
SVT
372
Allows you to quantify the amount of ST elevation and depression
J point
373
Causes the greatest risk of EMI
Coagulation setting of a MONOPOLAR CAUTERY.
