CV Conduction FINAL REVIEW Flashcards
1
Q
SA node is innervated by
A
SNS and PNS
2
Q
SA node blood supply comes from
A
Right Coronary Artery (RCA)
3
Q
% of people with SA node supplied by RCA
A
60%
4
Q
SA node 60% provided by RCA, remaining 40% supplied by
A
Left Circumflex Coronary Artery ( LCA)
5
Q
AV node innervated by
A
PNS and SNS
6
Q
AV node supplied by
A
RCA
7
Q
AV node supplied by RCA in what % of people
A
85-90%
8
Q
AV node 85-90% provided by RCA, remaining 10-15% supplied by
A
Left Circumflex Coronary Artery ( LCA)
9
Q
Both Right and Left Bundles receive Blood supply from branches of
A
Left Anterior Descending Coronary artery
10
Q
LAD infarcts affect_____and _____ but rarely______, why?
A
LAF and RBB ; LPF, it receives additional blood supply from posterior descending coronary artery
This is why LBB blocks (LBBB) indicate more extensive cardiac disease/damage
11
Q
LPF receives additional blood supply from
A
Posterior Descending coronary artery.
12
Q
Bifascicular heart block is present when
A
RBBB is present with Left anterior or posterior fascicular block. Anterior is more common because posterior gets dual blood supply and is larger.
13
Q
AV node allows time for
A
atrial contraction (atrial kick), which contributes an additional 20% to ventricular preload
14
Q
Automaticity changes when
A
phase 4 of depolarization shifts, or resting membrane
changes
15
Q
Automaticity changes: Sympathetic stimulation =
A
↑ slope of phase 4 of action potential and DECREASING resting membrane potential
16
Q
Automaticity changes: Parasympathetic stimulation =
A
↓ phase 4 of action potential and INCREASING RESTING MEMBRANE POTENTION
17
Q
Supraventricular (SVT) and urine
A
Polyuria can occur due to ↑ secretion of atrial natriuretic peptide
18
Q
SVT and ANP
A
Occurs because AV desynchrony causes atrial contraction against closed AV valves, resulting in ↑ atrial pressures activating stretch receptors → ANP released
19
Q
Triggered dysrhythmias c/ early after-depolarizations are
A
enhanced by slow heart rates and treated by
accelerating heart rate c/ drugs or pacing
20
Q
Triggered dysrhythmias c/ delayed after-depolarizations
are
A
enhanced by fast heart rates and can be treated c/
drugs that lower heart rate
21
Q
Sinus tachycardia and systemic diseases?
A
Most common supraventricular dysrhythmia associated c/ myocardial infarction (MI)
22
Q
Can be a compensatory physiologic effort to ↑ cardiac output (e.g. CHF)
A
Sinus Tachycardia
23
Q
Think twice
A
before treating tachycardia , may be a compensatory mechanism
24
Q
Sinus tachycardia treatment
A
Treat underlying cause
25
SVT (PACs) and systemic illness
Chronic Lung disease
IHD (ischemic heart disease)
digitalis toxicity
26
Pathologic increase in sympathetic tone
```
MI, CHF
PE
Hyperthyroidism
Pericarditis
MH
```
27
Heart beating too fast, secrete
ANP to decrease BV
28
MAT and systemic illness
Most commonly seen in ACUTE EXACERBATION of CHRONIC LUNG DISEASE
29
MAT and other related systemic illness
Methylxanthine toxicity (Theophyilline and caffeine)
Heart failure
Sepsis
Metabolic/ electrolyte abnormalities
30
Atrial Flutter : What is it ?
Atrial flutter (A-flutter) is an organized atrial rhythm c/ a rate of 250-350 bpm c/ varying degrees of AV block
31
Characteristics of Atrial flutter
Rapid P waves create a sawtooth appearance called flutter waves (especially noticeable in
leads II, III, aVF, and V1)
32
A flutter especially noticeable in
Leads II, III, aVF, and V1
33
With Aflutter: Ventricular rate may be
regular or irregular depending on rate of conduction
34
A-flutter Ventricular rate is normally about
150 bpm
35
A-flutter conduction
Most commonly, pts have 2:1 AV conduction (300
| atrial beats per 150 ventricular beats)
36
Untreated A-flutter can
Deteriorate to atrial fibrillation and revert back and forth
37
A-flutter is associated c/
structural heart disease
38
A-flutter can have
more intense symptoms than atrial fibrillation due to more rapid ventricular response
39
60% of pts get A-flutter c/ an acute exacerbation of a chronic condition such as (PIACET)
```
Pulmonary disease
Infarction (MI)
Acute myocardial
Cardiothoracic surgery , after surgery
Ethanol intoxication
Thyrotoxicosis
```
40
A-flutter that is hemodynamically significant is
treated c/ synchronized cardioversion
41
AFlutter that is hemodynamically stable
If hemodynamically stable, overdrive pacing can be used to convert to sinus rhythm
42
Pts c/ A-flutter lasting longer than
48 hours must be anticoagulated or should be evaluated by TEE for an atrial thrombus before cardioversion
43
When treating A-flutter pharmacologically, What is the initial goal?
Common meds to control ventricular rate
include amiodarone, diltiazem, and
verapamil
ventricular control is initial goal
44
WIth AFLUTTER, what are you preventing? Prevents
deterioration in AV conduction to 1:1, which would cause severe hemodynamic instability (procainamide is
used in this situation)
45
AFlutter just transitioned to 1:1 what medication can be used ?
Procainamide
46
AFlutter: Common meds to control ventricular rate
| include (VAD)
Verapamil
Amiodarone
Diltiazem
47
Anesthesia management for Aflutter
| Preop and Intraop
If it occurs spontaneously before induction, cancel case
| Intraoperative management depends on hemodynamic stability
48
Atrial fibrillation (A-Fib)occurs when
c/ a normal AV node, ventricular rates < 180
bpm
If AV node is bypassed, ventricular rates > 180
bpm (QRS complex is wide)
multiple areas of atria continuously depolarize and
| contract in a disorganized manner
49
AFib and rhythm coordination
No coordinated depolarization or contraction,
| only quivering atrial wall
50
AFib and Pwave
No discernable P waves
51
AFib and electrical input?
Irregular electrical input to AV node results in irregularly irregular ventricular contraction
52
Atrial fibrillation, with a normal AV node,
ventricular rates < 180 bpm
53
Atrial fibrillation, If AV node is bypassed,
ventricular rates > 180 bpm (QRS complex is wide)
54
Conditions that can lead to A-fib include: RHHICAPPA
Symptoms can be vague (generalized malaise)
or prominent, including palpitations, angina
pectoris, shortness of breath, orthopnea, and
HoTN
```
Rheumatic heart disease (especially mitral valve disease), HTN,
Hyperthyroidism,
IHD,
COPD
Alcohol intake (holiday heart syndrome)
Pericarditis
Pulmonary embolus
Atrial septal defect
```
55
ATRIA anatomy that correlate c/ A-fib
↑ left atrial size and mass
56
AFIB Symptoms can be G- PASOH
```
vague (generalized malaise) or prominent, including
Palpitations
Angina pectoris
Shortness of breath,
Orthopnea
HoTN
```
57
A-fib is most
common sustained cardiac dysrhythmia in general population
58
Incidence of AFIB
Increase with age
59
Most common underlying cardiovascular
| diseases associated c/ A-fib are
systemic HTN and IHD
60
Long-term A-fib
↑ risk of heart failure is most common sustained cardiac
| dysrhythmia in general population
61
AFib how does the conversion to thrombus occur
Loss of coordinated atrial contraction leads to stasis of blood and thrombus formation
62
2 most serious clinical dangers of A-fib
Atrial thrombi and thromboembolic stroke
63
AFIB patients require
Long-term prophylactic anticoagulation
64
AFIB Therapy goals include
ventricular rate control
| electrical or pharmacologic cardioversion
65
Drugs that slow AV nodal conduction: BCD
Side effects are dose related and most commonly
include AV block and ventricular ectopy
Beta Blockers
Calcium Channel Blocking drugs
Digoxin
66
AFIB, β-Blockers role -PPR
Prevent recurrent A-fib
Provide good heart rate control,
Reduce symptoms during subsequent episodes of A-fib
67
AFIB and Calcium channel–blocking drugs : 2 drugs use
(diltiazem, verapamil)
68
AFIB and Calcium channel–blocking drugs role
can rapidly reduce ventricular rate during A-fib
69
AFIB and CCBs, caution
CCBs, Have negative inotropic effects and must be used c/ caution in heart failure
70
AFIB and Digoxin
can used to control ventricular rate but is not effective for conversion of atrial fibrillation to sinus rhythm.
71
AFIB and digoxin and acute setting use
In acute settings, usefulness is limited due peak therapeutic effects being delayed by several hours
72
AFIB and digoxin Side effects are
Dose related and most commonly include AV block and ventricular ectopy
73
AFIB and Pharmacological cardioversion
is most efficacious if initiated within 7 days of onset
74
AFIB: What are Drugs capable of converting A-fib? include: APIS
Amiodarone
Propafenone
Ibutilide
Sotalol
75
For Treatment of AFIB, when is Amiodarone preferred?
Is preferred in pts c/ significant heart disease (IHD, LVF, left ventricular dysfunction, and heart failure)
76
AFIB: Amiodarone Action
suppresses atrial ectopy and recurrence of atrial fibrillation and improves success rate of electrical cardioversion
77
AFIB and Cardioversion
Electrical cardioversion is most effective method for converting A-fib to normal sinus rhythm and is indicated in
78
AFIB, when is cardioversion indicated? (HAH)
pts c/ coexisting symptoms of heart failure, angina
| pectoris, or hemodynamic instability
79
Intraoperative management of A-fib depends
on hemodynamic stability
80
Intra-operative AFIB Instability is treated c/
synchronized cardioversion 100-200J biphasic
81
Intra-operative AFIB if vitals are stable, rate control can be achieved with
c/ β-Blockers and calcium channel blockers
82
Intraoperative management of A-fib: DRUGS
Procainamide or amiodarone are drugs of choice to control rate in a pt c/ known or suspected electrical accessory pathway and pre-excitation
83
AFIB: INTRAOP may be attempted if vital signs allow:
Pharmacologic conversion to sinus rhythm c/ IV
| amiodarone –> Can result in bradycardia, HoTN
84
A-fib is most common
postoperative tachydysrhythmia, occurring early (first 2-4 days)
85
CHRONIC AFIB and medication
Pts c/ chronic A-fib should continue antidysrhythmic drugs perioperatively
86
AFIB and electrolytes monitoring
Check magnesium and potassium levels (especially if
| on digoxin)
87
AFIB and team
Coordination c/primary care team is needed to manage anticoagulation
88
Ventricular Pre-excitation Syndromes
Alternate (accessory) conduction pathways can function as electrically active muscle bridges bypassing normal
conduction pathways and providing a pathway for re-entrant tachycardias
89
Example of Ventricular Pre-Excitation syndromes
Wolff-Parkison-White (WPW)
90
What is Wolff-Parkinson-White (WPW) syndrome cause?
caused by an accessory pathway between atria and ventricles, called bundle of Kent
91
In WPW Impulses in
bundle of Kent can cause PVCs that can result in a unique type of SVT (Atrioventricular nodal re-entrant Tachycardia)
92
WPW Common in pts
Transposition of great vessels
Hypertrophic cardiomyopathy, and
Ebstein’s malformation
93
WPW Symptoms include: PADS DP
```
Paroxysmal palpitations
Angina
Dizziness,
Syncope,
Dyspnea
Pectoris
```
94
Evident on ECG for WPW
Delta wave
95
WPW is diagnosed when
both pre-excitation and
| tachydysrhythmias are present
96
WPW is diagnosed when both pre-excitation and
| tachydysrhythmias are present: Pre-excitation causes an
earlier deflection of QRS called a delta wave
97
WPW _______is commonly triggered by a PAC
Atrioventricular nodal re-entrant tachycardia (AVNRT)
98
WPW antidromic,
cardiac impulses are conducted from atrium to ventricle via accessory pathway and return from ventricles to atria via normal AV node
99
WPW Drugs Contraindicated:
```
SLOW AV nodal conduction ↑ conduction along
accessory pathway (and are contraindicated
```
100
Drugs contraindicated with WPW that slow AV node conduction and increase accessory pathway? ABCDL
```
Adenosine
β-blockers,
Calcium channel blockers
Digoxin
Lidocaine
```
101
Orthodromic AVRT
Antegrade conduction through AV node
102
Antidromic AVRT
Retrograde conduction through AV node.
103
WPW ↑
conduction along accessory pathway
| produces a rapid ventricular rate (V-Tach/Fib)
104
WPW treatment drug and its mechanism of aciton
Treatment: procainamide 10mg/kg IV
| Slows conduction along accessory pathway and slows ventricular response
105
WPW if drug therapy fails?
Cardioversion is indicated if drug therapy fails
106
WPW , other arrythmias that can lethal -->
A-fib/flutter c/ WPW can be lethal because impulses will conduct via accessory pathway and cause very rapid ventricular rates that can deteriorate to V-Fib
107
A-Fib/Flutter c/ WPW should be treated c/
procainamide
108
A-Fib/Flutter c/ WPW drugs contraindicated and why?
Verapamil and digoxin are contraindicated because
| they accelerate conduction through accessory pathway
109
WPW If hemodynamically unstable_________, what may be necessary?
cardioversion ; Radiofrequency catheter
| ablation may be necessary
110
Pts c/ WPW should continue their
antidysrhythmic medications intraoperatively
111
WPW Anesthesia management involves
minimizing any event (e.g. ↑ sympathetic nervous system activity) or drug (digoxin, verapamil) that enhances conduction of impulses via accessory pathway
112
What is a BBB?
Conduction disturbances at various levels of His-Purkinje system
113
BBB is usually associated with
significant structural heart disease, especially dilated
| cardiomyopathies
114
Clinical significance of Right bundle branch block (RBBB)
Does not always imply cardiac disease and often of
| no clinical significance
115
RBBB can be related to (VIA)
Valvular heart disease
IHD
Atrial septal defect
116
RBBB is recognized on ECG by a WR1,2
| DS 1 V6
widened QRS complex and
| rSR’ configuration in leads V1 and V2, deep S wave in leads I and V6
117
Bifascicular heart block is present when
RBBB is present c/ left anterior or posterior fascicular block (anterior is more common because posterior gets dual blood supply and is larger)
118
Complete RBBB, Lead I
Wide Slurred S wave in Lead I
119
Complete RBBB, Lead V1
Terminal R wave in V1 (R, rR', rsR',
120
Normal in RBBB
T wave inversion
| and ST depression in V1-V3
121
Complete RBBB, Lead V6
Slurred S wave
| S wave should be > duraton then the R wave or greater than 40ms in V1 and V6 in adults.
122
Left bundle branch block (LBBB) is recognized on ECG as
a QRS complex of longer than 0.12 seconds in duration and absence of Q waves in leads I and V6
123
LBBB waves
Broad notched or slurred R wave in leads I, aVL, V5, and V6 and an occasional RS pattern in V5 and V6
124
LBBB classification
Can be classified as unifascicular (hemiblock) or
| complete
125
LBBB is often associated c IHV
/ IHD, HTN, and valvular heart disease
126
Complete LBBB ECG Lead I: LIMB LEADS
T wave discordance
| Monophasic QRS in left sided leads
127
Complete LBBB ECG lead V1:
Right sided leads
NEGATIVE QRS Right sided leads
QRS > 0.12
128
Complete LBBB ECG lead V6
Left sided chest leads
Monophasic QRS
Left sided Leads
129
Appearance of LBBB during anesthesia,
particularly during hypertensive or tachycardic
| episodes, may be a sign of myocardial ischemia
130
LBBB is a
marker of serious heart disease (CAD, aortic valve disease, cardiomyopathy)
131
Third-degree heart block can occur
if a central line catheter induces RBBB in a pt c/ preexisting LBBB
132
RBBB (usually transient) occurs during
insertion of a pulmonary artery catheter in approximately 2% to 5% of pts
133
Surgery c/ Cardiac Implantable Devices
Complications that can occur related to
automatic implantable cardioverterdefibrillator (AICD) include: TBHMM DDR
Tachydysrhythmias or
Bradydysrythmias,
HoTN,
myocardial damage,
myocardial ischemia or infarction,
device malfunction, delay or cancellation of
surgery, readmission to a health care facility
134
Surgery c/ Cardiac Implantable Devices: If pt has a device, they have one of following: THOROUGH ASSESSMENT
bradydysrhythmia,
| tachydysrhythmia, or heart failure
135
Surgery c/ Cardiac Implantable Devices: If pt has a device, they have one of following: bradydysrhythmia,
tachydysrhythmia, or heart failure
Preoperative assessment should include (TICAA)
```
Type of device present
Identification of
Clinical indication for device
Appraisal of patient’s degree of dependence on
device, and
Assessment of device function
```
136
Surgery c/ Cardiac Implantable Devices
| Syncope
in a pt c/ a pacemaker could reflect device dysfunction
137
Surgery c/ Cardiac Implantable Devices What Indicates pulse generator function?
Rate of discharge of an atrial/ventricular
| asynchronous (fixed-rate) cardiac pacemaker (usually 70 bpm)
138
Surgery c/ Cardiac Implantable Devices may reflect battery depletion
10% ↓ from baseline
139
Surgery c/ Cardiac Implantable Devices :An irregular rate could indicate
Competition of pulse generator c/ patient’s intrinsic heart rate, or failure of pulse generator to sense R waves
140
Best way to determine AICD function preoperatively is
AICD interrogation by a qualified consultant
141
Surgery c/ Cardiac Implantable Devices Due to comorbidities of pts c/ AICD (CAD, HTN, DM), good clinical outcomes depend on
Evaluation and optimal treatment of co-existing diseases in addition to management of issues directly
involving AICD
142
Most common CIED-related problem
| encountered in perioperative period
```
is interference c/ device function resulting from
electromagnetic interference (EMI)
```
143
EMI Most common effects are
inhibition of pacing and resetting of device to asynchronous pacing
144
EMI can cause
inappropriate defibrillation or complete device failure
145
Procedures that have reported EMI-induced
| dysfunction are
MR
Electrocautery,
Radiofrequency ablation,
146
Anesthesia usually will not directly effect aes
AICD, but physiologic changes (acid-base,
electrolytes) and hemodynamic shifts (heart rate, heart rhythm, HTN, coronary ischemia) can induce changes in AICD function and adversely affect pt outcomes
147
Most literature suggests Doing this before surgery?
reprogramming AICD to an asynchronous mode before surgery if pt is pacemaker dependent (magnet)
148
Use of monopolar electrocautery remains
principal concern intraoperatively in pts c/ AICD
149
This causes more EMI problems?
Use of “coagulation” settings in monopolar
electrocautery causes more EMI problems
than use of “cutting” settings
150
Keep electrocautery current
as low as possible and applied in short bursts, especially if near pulse generator
151
SCAPEL and EMI
bipolar electrocautery or ultrasonic Harmonic scalpel is associated c/ lower rates of EMI effects on pulse generator and leads
152
EMI and Grounding pad
should be placed so that current path does not cross chest or AICD system
153
Pacemaker rate and function
Application of a magnet to a pacemaker often
results in asynchronous pacemaker function at a
fixed rate
154
Magnet must
MUST remain in place to maintain asynchronous
mode of pacing, and removal of magnet results in
reversion to baseline program
155
Application of a magnet to a cardioverter defibrillator
rarely alters pacing capabilities, but most often suspends antitachycardia therapy (defibrillation)
156
Some ICDs have
no magnet response; others can
| be permanently disabled by magnet exposure
157
Recommendations for pts c/ ICDs who undergo a
| procedure c/ a high risk of EMI include
turning off defibrillator and electronically adjusting pacing
modes as appropriate in pacemaker-dependent
individuals.
158
Temporary transvenous cardiac pacemakers
| create a situation in which there is a
direct connection between an external electrical source
| and endocardium.
159
Risk of Vfib resulting from
microshock
160
Risk of lead dislodgment is
minimal a month or longer after lead implantation
161
Recommendations for pts undergoing lithotripsy include
keeping focus of lithotripsy beam away from pulse
| generator
162
Potential AICD problems from radiation therapy include
pacemaker failure and “runaway” pacemaker
163
Sudden rapid and erratic pacing
multiple internal component malfunctions
164
Before electroconvulsion therapy, device
| should be
interrogated and antitachycardia
| functions suspended
165
In pacemaker-dependent pts, programming to
asynchronous mode is recommended
166
Other potential sources of EMI during anesthetic care include CELSM
```
Current from peripheral nerve stimulators
Evoked potential monitors
Large tidal volumes
Shivering, and
Medication-induced muscle fasciculations
```
167
If emergency defibrillation is necessary in
| a pt c/ a AICD, what to do? Where to place electrodes?
defibrillation current should be kept away from pulse
| generator and lead system. Place electrode pads in an anterior– posterior position
168
What may follow external defibrillation?
An acute ↑ in pacing threshold and loss of capture –> Transcutaneous cardiac pacing or temporary transvenous pacing may be required
169
Postop management of pt c/ a AICD consists of
| postoperative period, including during transport
interrogating device and restoring appropriate baseline
| settings
170
POSTOP interrogation of the device should be done when?
Should be done as soon as possible after procedure
171
Implantaable devices, should be monitored throughout?
Cardiac rate and rhythm should be monitored throughout
| immediate
172
Postoperative interrogation may NOT BE NEEDED if:
| No EBIS
surgery did not use EMI-generating devices
no electronic preoperative device reprogramming was
done,
no blood transfusions were administered, and
no intraoperative problems were identified that related to
AICD function
