Cardiac rhythm monitors and equipment Flashcards
1
Q
Conduction varies through different tissues.
Slow, Intermediate, or Fast. Which are which?
SA/AV nodes, Bundle of His and Purkinje fibers, myocardial muscle cells
A
SA/AV: Slow
Myocardial muscle cells: Inter
Bundle of His and Purkinje: Fast
2
Q
Name 4 accessory pathways
A
James fiber
Atrio-hisian fiber
Kent’s bundle
Mehaim bundle
3
Q
What does the absolute refractory period mean?
A
Means that no stimulus (no matetr how strong) can depolarize the myocyte
4
Q
Wha does the relative refractory period mean?
A
Means that a larger than normal stimulus is required to depolarize the myocyte
5
Q
What is considered the isoelectric line and therefore used as a reference point for measuring ST elevation and depression?
A
PR interval
6
Q
What is considered the J point?
A
Where the QRS complex ends and the ST segment begins.
7
Q
ST depression/elevation can be determined by comparing the _ to the _
A
j point
PR interval
8
Q
As a general rule, how much difference is considered significant when it comes to ST elevation or ST depression?
A
+1.0
-1.0
9
Q
If K is too high, what change can it make on the EKG?
A
Narrow and peaked T wave
Short QR
Wide QRS
Low P amplitude
Wide PR
Nodal block
Sine wave fusion of QRS and T –> VF or asystole
*In order of appearance from early to late)
10
Q
If K is too low, what changes will be seen on the EKG?
A
U wave
ST depression
Flat T wave
Long QT
11
Q
What EKG change is seen for too high of Ca++?
A
Short QT
12
Q
What EKG change is seen for too low of Ca++?
A
Long QT
13
Q
What changes to EKG are seen if Mg ++ is too high?
A
No significant effect unless very high which would lead to heart block, cardiac arrest
14
Q
What changes to EKG are seen if Mg ++ is too low?
A
No significant effect unless very low which could lead to long QT
15
Q
A + deflection occurs when the vector of depolarization travels towards the (+ or -) electrode
A
+
16
Q
A - deflection occurs when the vector of depolarization travels away from the (+ or -) electrode
A
+
17
Q
A biphasic deflection occurs when the vector of depolarization travels in what relation to the + electrode?
A
Perpendicular
18
Q
The heart depolarizes from the: apex to base or base to apex?
A
Base -> apex
19
Q
The heart depolarizes from the: endocardium to the epicardium or the epicardium to the endocardium?
A
Endo -> epi
20
Q
Vector of Depolarization is represented by which portion of the EKG?
A
QRS
21
Q
Vector of Repolarization is represented by which portion of the EKG?
A
T wave
22
Q
The heart repolarizes from apex to base or base to apex?
A
Apex -> base
23
Q
The heart repolarizes from epicardium to endocardium or endocardium to epicardium?
A
Epi-> Endo
24
Q
Why is the T wave upright?
A
Due to a double negative. Its a negative electrical current traveling in the opposite direction as the vector of depolarization.
25
Which leads are the bipolar leads?
I II III
26
Which leads are the limb leads?
aVR, aVL, aVF
27
Which leads are the precordial leads?
V1-V6
28
What degree windows represent left axis deviation, normal axis, right axis, extreme right axis
Left: -30 to -90
Normal: +90 to -30
Right: +90 to +180
Extreme right: -90 to +180
29
With a normal axis, what is the positioning of lead I and aVF? (upright or down?)
I: up
AVF: up
30
With a left axis deviation, what is the positioning of lead I and aVF? (upright or down?)
I: +
AVF: +
31
With a right axis deviation, what is the positioning of lead I and aVF? (upright or down?)
I: down
aVF: up
32
With an extreme right axis deviation, what is the positioning of lead I and aVF? (upright or down?)
I: down
AVF: down
33
A normal axis is between how many degrees?
-30 and +90
34
Left axis deviation is more - than __ degrees
-30
35
Right axis deviation is more + than __ degrees
90
36
The mean electrical vector tends to point towards or away from areas of MI?
Away
37
Does the following factor cause Right or Left axis deviation?
COPD
Right
38
Does the following factor cause Right or Left axis deviation?
Acute bronchospasm
Right
39
Does the following factor cause Right or Left axis deviation?
Pulm HTN
Right
40
Does the following factor cause Right or Left axis deviation?
PE
Right
41
Does the following factor cause Right or Left axis deviation?
Chronic HTN
Left
42
Does the following factor cause Right or Left axis deviation?
LBBB
Left
43
Does the following factor cause Right or Left axis deviation?
Aortic stenosis
Left
44
Does the following factor cause Right or Left axis deviation?
Aortic insufficiency
Left
45
Does the following factor cause Right or Left axis deviation?
Mitral regurg
Left
46
What usually causes sinus arrhythmia?
When the SA nodes pacing rate varies with respiration.
It is usually benign.
47
Sinus arrhythmia is due to which reflex?
Bainbridge
48
How does inhalation cause increased HR with sinus arrythmia?
Inhalation -> decreased intrathoracic P -> Increased venous return -> increased heart rate
49
How does exhalation cause decreased HR with sinus arrhythmia?
Exhalation -> increased intrathoracic P -> Decreased venous return -> Decreased heart rate
50
Underdosing Atropine can cause paradoxical bradycardia below what dose?
< 0.5 mg
51
What can be given for CCB or BB OD? Dose?
Glucagon
50-70 mcg/kg q 3-5 min
Followed by an infusion at 2-10 mg/hr
52
What energy should cardioversion be delivered for acute onset afib?
100 J
53
If the onset of afib/aflutter is older than 48 hours (or if onset is undetermined, a TEE must ne performed to rule out what?
Atrial thrombus
54
Is new onset or undiagnosed a fib an indication to cancel surgery?
YES! They could have a clot
55
What is the most common post op tachydysrythmia especially in older patients after cardiothoracic surgery?
afib
56
Hemodynamically unstable a flutter with cardioversion should start at what energy?
50 J
57
Rate for AV node
40-60
58
Where would a PVC have to hand to precipitate the R on T phenomenon?
On the second half of the T wave (during the relative refractory period)
59
When is the decision made to treat PVC's?
When they are frequent (> 6/min), polymorphic, or when they occur in runs of 3 or more
60
Lidocaine dosing for symptomatic PVCs?
1-.1.5 mg/kg
If PVCs continue, follow with a gtt of 1-4 mg/min
61
Patients with Brugada syndrome have a pseudo right or left BBB? Persistent elevation in which leads?
V1-V2
62
What ion channel is to blame for Brugada syndrome?
Sodium
63
What is a cause of sudden nocturnal death due to VT or VF?
Brugada syndrome
64
Brugada syndrome is most common in which population?
Males in Southeast Asia
65
What protective measures should be taken for the patient with Brugada syndrome as they undergo surgery?
ICD or pad placement during surgery
66
What is considered a first degree heart block?
PR interval > 0.20 sec
67
What region is affected leading to first degree heart block?
AV node or Bundle of His
68
Etiology of first degree heart block?
Age related degenerative changes, CAD, digoxin, amiodarone
69
Tx for first degree AV block?
Monitor
(usually asymptomatic)
70
What is second degree heart block type 1?
Longer, longer, longer, drop then you have a Wenckebach
71
Affected region for 2nd degree AV block type 1
AV node
72
Etiology of 2nd degree heart block type 1
Structural conduction defect
MI
BB
CCB
Dig
Sympatholytic agents
73
Tx for second degree heart block type 1
If asymptomatic -> safe to just monitor
If symptomatic -> Atropine
74
What is second degree heart block type 2?
If some P's do not get through, you have a Mobitz type II
Usually a 2:1 or 3:1 ratio
75
Affected region for 2nd degree heart block type 2?
His bundle or bundle branches
76
Etiology of second degree heart block type 2?
Structural conduction defect or infarction
77
Treatment of second degree heart block type 2?
Often symptomatic (palpitations and syncope)
Pacemaker (transcutaneous, transvenous, or implantable)
Atropine is often not effective
78
What is the big danger of 2nd degree heart block type 2 in terms of progression?
It can progree to complete heart block
79
What is a 3rd degree heart block?
If Ps and Qs don't agree then you have a Third Degree
AV dissociation
80
Etiology of 3rd degree heart block
Fibrotic degeneration of the atrial conduction system, Lenegre's disease
81
Treatment of 3rd degree heart block
Pacemaker (transcutaneous, transvenous, implantable)
Isoproterenol (chemical pacemaker)
82
What is Stokes Adams attack related to 3rd degree heart block?
Decreased CO -> decreased cerebral perfusion -> syncope
83
MOA of class 1 anti arrhythmics
Na Channel Blockers
84
MOA of class 2 anti arrhythmics
Beta blockers
85
MOA of class 3 anti arrhythmics
K channel blockers
86
MOA of class 4 anti arrhythmics
Ca channel blockers
87
How many different subclasses are there of Na channel blockers? What are they?
3
1A
1B
1C
88
MOA of Na channel blockers
Depression of phase 0
89
Which drugs fall under 1A Na channel blockers?
Quinidine
Procainamide
Disopyramide
90
Which drugs fall under 1B Na channel blockers?
Lidocaine
Phenytoin
91
Which drugs fall under 1C Na channel blockers?
Flecainide
Propafenone
92
MOA of Beta blockers?
Slows phase 4 depol in SA node
93
MOA of K channel blockers?
Prolongs phase 3 repol
Increases effective refractory period
94
MOA of CCB
Decrease conduction velocity through AV node
95
Which drugs fall in K+ channel blockers?
Amio
Bretyium
96
How to dose Amio through peripheral IV (dose)
6 then 12 mg
97
How to dose Amio through central line (dose)
3 mg then 6 mg
98
Caution should be taken with patients with what comorbidity before giving adenosine?
Asthma
Bronchospasm
99
What 2 rhythms might Amio be good for
SVT and WPW with a norrow QRS.
NOT AF AFlutter or VTACH
100
How quickly is Adenosine metabolized and where
Rapidly.
t 1/2 = 5 seconds
101
Why does reentry not usually occur with a normal pathway
The impulse moves forward and cannot move backwards, because all the tissues behind the impulse remain in the refractory period
102
How does impulse move through a reentry pathway?
One pathway is normal and the other has a unidirectional block. The impulse cannot move past the block but if it comes from the back side it can
*Remember there are connecting pathways
*By the time the impulse comes around, those cells have recovered and allow additional depol
103
What are the 2 ways to disrupt the reentry circuit?
1. Slow conduction velocity through the circuit
2. Increase the refractory period of the cells at the location of the unidirectional block
104
WPW is a syndrome that allows the impulse to bypass which structure in the heart? What does that lead to?
AV node
AV node is usually responsible for slowing the impulse down before it enters the ventricle
In this case, the impulse is not slowing down and it is going from the atria to the ventricle quicker through an accessory pathway bypassing the AV node, the impulse also goes through the AV node, so when that impulse finally reaches the ventricle it will cause a change on the EKG
105
What are some things seen on the EKG with WPW?
Delta wave
Short PR interval
Wide QRS complex
Possible T wave inversion
106
What is the cause of delta wave on EKG?
The accessory pathway moves the impulse from the atria through the ventricle quickly which depolarizes it, but the impulse also moves through the AV node. When the impulse from the AV node catches up, it causes a change in the slope of the QRS --> delta wave
107
What is the most common tachy-dysrhythmia associated with WPW
AV nodal reentry tachycardia
108
What are the 2 types of AV nodal reentry tachycardias?
Orthodromic
Antidromic
109
Which of the 2 types of AV nodal reentry tachycardias is more common?
Orthodromic > Antidromic
110
How does signal pass through the heart with orthodromic AV node reentry tachycardia
Atrium -> AV node -> Ventricle -> Accessory pathway -> atrium
111
How does signal pass through the heart with antidromic AV node reentry tachycardia
Atrium -> Accessory pathway -> Ventricle -> AV node -> Atrium
112
Is QRS narrow or wide with antidromic AV node reentry tachycardia
wide
113
Is QRS narrow or wide with orthodromic AV node reentry tachycardia
narrow
114
Where should you block the conduction impulse with orthodromic AVNRT?
At the AV node
115
Where should you block the conduction impulse with antidromic AVNRT?
accessory pathway
116
What is the treatment (drugs & interventions) for orthodromic AVNRT?
Cardioversion
Vagal maneuvers
Adenosine
Beta blockers
Verapamil
Amio
117
What is the treatment (drugs & interventions) for antidromic AVNRT?
Cardioversion
Procainamide
118
Which of the 2 types of AVNRT is the most dangerous?
antidromic
This is because the gatekeeper function of the AV node is bypassed and the heart rate can increase well beyond the heart's pumping abil
119
If the patient with WPW has afib, the drug tx of choice works to increase the refractory period of the accessory PW or AV node?
Procainamide to increase the refractory period in the accessory pathway
120
What is the definitive treatment for WPW?
Ablation of the accessory pathway
121
What is torsades de pointes?
Polymorphic ventricular tachycardia
122
What rhythm can R on T cause
V tach
TDP
123
What change on the EKG is associated with torsades de pointe?
Long QT interval
124
Which electrolyte disturbances prolong the QTc?
Hypokalemia
Hypocalcemia
Hypomagnesemia
125
Which drugs cause a prolonged QTC interval?
Methadobe
Droperidol
Haloperidol
Ondansetron
Halogenated anesthetics
Amiodarone (esp with hypokalemia)
Quinidine
126
Genetic syndromes associated with a long QT interval
Romano Ward syndrom
Timothy syndrom
127
What is considered a prolonged QT interval? Male vs Female
Male: > 0.45 sec
Female: > 0.47
128
Pacemakers are categorized by a 5 letter code. What does each stand for?
PaSeR
1: Chamber Paced
2: Chamber Sensed
3: Response
4: Programability options
5: Indicates the pacemaker can pace multiple sites
128
What are the different options position 1 could be- the chamber that is paced?
O=None
A=Atrium
V=Ventricle
D=Dual
129
What are the different options position 2 could be- the chamber that is sensed ?
O=None
A=Atrium
V=Ventricle
D=Dual
130
What are the different options position 3 could be- the response to sensed native cardiac activity?
O=None
T= Triggered (sensed activity tells the PPM to fire)
I= Inhibited (Sensed activity tells the PPM NOT to fire)
D=If native activity is sensed, then pacing is inhibited. If native activity is not sensed, then the pacemaker fires
131
What are the different options position 4 could be- programmability of the PPM?
O=None
R=Rate modulation
132
What would be 3 example of asynchronous pacing?
AOO
VOO
DOO
132
What is asynchronous pacing?
Pacemaker does not sync with the patient's heart rate or rhythm. It gives constant impulses regardless of underlying rhythm
133
What is single chamber demand pacing?
Think of this as a backup mode- it only fires when the native heart rate falls below a predetermined rate
134
What would be 3 example of single chamber demand pacing?
AAI
VVI
Sensed activity tells the pacemaker NOT to fire
135
What happens when you place a magnet over a pacemaker?
Usually (but not always) converts the pacemaker to an asynchronous mode.
*The best answer is to consult with the manufacturer to determine how a magnet affects the pacemaker
136
What happens when you place a magnet over an ICD?
Suspends the ICD and prevents shock delivery
137
What happens when you place a magnet over a pacemaker + ICD?
Suspends the ICD and prevents shock delivery
Has NO effect on the pacemaker function.
138
Pacemakers can fail in what 3 ways?
1. Failure to sense
2. Failure to capture
3. Failure to output
139
What is failure to sense?
PPM fails to sense underlying rhythm and sends an impulse at sporadic times
140
What is the big worry around failure to sense?
Failure to sense can lead to R on T -> V tach
141
What is failure to capture
When the PPM provides a pacing spike but the atria or ventricle doesn't respond to it
142
What can cause failure to capture besides electrode displacement or wire fracture?
Conditions that make the myocardium more resistant to depolarization or a reduction of electronegativity such as:
High or low K
Low CO2 (intracellular K shift)
Hypothermia
MI
Fibrotic tissue buildup around the pacing leads
Antiarrythmic meds
143
What is failure to output
Failure to output occurs when a pacing stimulus is not produced in a situation when it should be produced
144
What is EMI in regards to pacemaker?
Electromagnetic interference which can disrupt the pacemaker function
145
When electrocautery is used, which setting causes more EMI? Coagulation or cutting setting?
Coagulation
146
Does mono or bipolar cautery cause more EMI?
Mono
147
If the surgeon insists on using monopolar in a patient with a PPM or ICD what can you suggest?
He or she use short bursts < 0.5 sec
148
The risk of EMI is highest when the electrocautery tip is used within a ___ cm radius of the pulse generator.
15
149
Where should the electrocautery return pad be placed with PPM or AICD?
Far away from the pulse generator and in a location that prevents a direct line or current through the pulse generator
150
What is the single most important bit of information you need to know about a patients PPM in preop?
What the underlying rhythm is in case the pacemaker fails to work
151
